Publications by authors named "Xiao-Mei Lu"

60 Publications

[Expression of long non-coding RNA linc00467 in childhood acute myeloid leukemia and its role in drug resistance].

Zhongguo Dang Dai Er Ke Za Zhi 2020 Jul;22(7):734-738

Key Laboratory of Genetics and Infectious Diseases, Dongguan Institute of Pediatrics, Dongguan, Guangdong 523327, China.

Objective: To study the expression and function of long non-coding RNA linc00467 in childhood acute myeloid leukemia (AML).

Methods: Bone marrow samples were collected from 5 children with AML who were diagnosed from May 2016 to June 2018. Normal bone marrow samples based on bone marrow examination were collected from 3 children as controls. Quantitative real-time PCR was used to measure the expression of linc00467 in the two groups. A lentivirus system was used to achieve overexpression of linc00467 in AML cells (HL-60) (linc00467 overexpression group), and empty vector expressing green fluorescent protein (GFP) was transfected into AML cells to establish a GFP control group. A lentivirus system was used to insert an interfering sequence into AML cells (sh-linc00467 interfering group), and a random sequence was inserted to establish an sh-NC control group. Cell proliferation and resistance to doxorubicin were observed for all groups.

Results: Compared with the normal control group, the children with AML had a significant increase in linc00467 (P=0.018). Overexpression and interference with linc00467 expression had no significant effect on cell proliferation. Compared with the GFP control group, the linc00467 overexpression group had a significant increase in the viability of HL-60 cells at the adriamycin concentrations of 0.1, 0.2, 0.3, 0.4, and 0.5 μg/mL (P<0.05). Compared with the sh-NC control group, the sh-linc00467 interfering group had a significant reduction in the viability of HL-60 cells at the adriamycin concentrations of 0.1, 0.2, 0.3, 0.4, and 0.5 μg/mL (P<0.05). Compared with the untreated group, the adriamycin treatment group had a significant increase in the expression of linc00467 in HL-60 cells (P<0.05).

Conclusions: This study reveals the biological function of linc00467 to promote the resistance to adriamycin in AML, which provides a basis for developing new therapeutic drugs for AML.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7389624PMC
July 2020

is associated with lymph node metastasis in esophageal squamous cell carcinoma.

Oncol Lett 2016 Dec 2;12(6):5223-5228. Epub 2016 Nov 2.

Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830011, P.R. China; State Key Lab Incubation Base of Xinjiang Major Diseases Research, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830011, P.R. China.

, of which there are few studies regarding cell biology and neurological diseases, has been found to be significantly amplified in esophageal squamous cell carcinoma (ESCC) with lymph node metastasis compared with ESCC without lymph node metastasis. This suggests that may play a role in the lymph node metastasis of ESCC. There has, to the best of our knowledge, been no study performed to investigate the role of in ESCC. In the present study, the expression of was detected by immunohistochemistry, and its expression was statistically analyzed with clinicopathological parameters, using commercially obtained tissue arrays consisting of 86 cases of ESCC and 79 paired controls. was knocked down using transient transfection with specific small hairpin RNA (shRNA) vectors into ESCC TE-1 and EC9706 cell lines whose endogenous level was highest. The variation of proliferation, migration and invasion were evaluated using methyl thiazolyl tetrazolium, wound healing and Transwell assay, respectively. It was found that expression was significantly associated with lymph node metastasis and differentiation, and that knockdown of cannot significantly affect proliferation and mobility in the ESCC cell line TE-1. Overall, this is the first study suggesting that may play a role in the lymph node micrometastasis of ESCC.
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http://dx.doi.org/10.3892/ol.2016.5343DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5279220PMC
December 2016

Candidate single-nucleotide polymorphisms and cerebral palsy: A case-control study.

Biomed Rep 2015 Nov 25;3(6):849-852. Epub 2015 Sep 25.

Department of Pediatrics, Dongguan Children's Hospital, Dongguan, Guangdong 523325, P.R. China ; Dongguan Institute of Pediatrics, Dongguan, Guangdong 523325, P.R. China.

Certain genetic polymorphisms have been suggested to be associated with cerebral palsy; the candidate genes are involved in thrombophilia, inflammation and preterm labor, but the mechanism remains to be elucidated. The aim of the present study was to investigate the associations between selected single-nucleotide polymorphisms (SNPs) and cerebral palsy among children. A case-control study was conducted, including 74 infants with cerebral palsy (case group) and 99 healthy infants (control group). The distributions of the allele and genotype frequencies were examined for the total cerebral palsy patient population in addition to subgroups divided according to gestational age (preterm versus full-term). The results showed that the rs1042714 variant in adrenergic receptor β-2 () and heterozygosity for were associated with the cerebral palsy risk among the preterm infants. No significant differences in the allele or genotype frequencies were observed between the total cerebral palsy patient population and controls for the eight SNPs investigated.
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http://dx.doi.org/10.3892/br.2015.519DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4660632PMC
November 2015

Lumican overexpression exacerbates lipopolysaccharide-induced renal injury in mice.

Mol Med Rep 2015 Sep 16;12(3):4089-4094. Epub 2015 Jun 16.

Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

The present study aimed to investigate the role of lumican in mice with endotoxin-induced acute renal failure (ARF). Lumican transgenic mice and wild‑type mice were injected with lipopolysaccharide (LPS; 10 mg/kg) to establish a model of ARF. The mice were sacrificed at 24 h and the blood and renal tissue samples were collected. The value of serum creatinine (SCr) and blood urea nitrogen (BUN) were measured to determine renal function. An ELISA was used to determined the concentrations of renal cytokines, including tumor necrosis factor (TNF)α, interleukin (IL)‑6, IL‑4 and IL‑10. The protein expression levels of Toll-like receptor (TLR4) and nuclear factor (NF)κB in renal tissues were assessed using western blot analysis. Terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling was performed to monitor apoptosis of renal tissue. Light microscopy and electron microscopy were used to observe structural changes in the renal tissues. Following the administration of LPS, the SCr and BUN values of mice in the lumican transgenic group were higher compared with those in the control group. The expression levels of renal TLR4, NFκB, TNFα, IL‑6, IL‑4 and IL‑10 were upregulated in the lumican transgenic mice compared with those in the wild‑type control group. Apoptosis was detected predominantly on the renal tubule. There was a significant difference in the optical density of apoptotic bodies between the control mice and the lumican transgenic mice. Light and electron microscopy demonstrated more severe renal tissue injury in the lumican transgenic mice compared with that in the control mice. In conclusion, LPS may cause excessive apoptosis in the renal tubular cells via the TLR4 signal transduction pathway, a decrease in the number of renal tubular cells and ARF. Lumican may be important in mice with LPS-induced ARF.
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http://dx.doi.org/10.3892/mmr.2015.3940DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526055PMC
September 2015

Establishing a Nomogram for Stage IA-IIB Cervical Cancer Patients after Complete Resection.

Asian Pac J Cancer Prev 2015 ;16(9):3773-7

Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China E-mail :

Background: This study aimed to establish a nomogram by combining clinicopathologic factors with overall survival of stage IA-IIB cervical cancer patients after complete resection with pelvic lymphadenectomy.

Materials And Methods: This nomogram was based on a retrospective study on 1,563 stage IA-IIB cervical cancer patients who underwent complete resection and lymphadenectomy from 2002 to 2008. The nomogram was constructed based on multivariate analysis using Cox proportional hazard regression. The accuracy and discriminative ability of the nomogram were measured by concordance index (C-index) and calibration curve.

Results: Multivariate analysis identified lymph node metastasis (LNM), lymph-vascular space invasion (LVSI), stromal invasion, parametrial invasion, tumor diameter and histology as independent prognostic factors associated with cervical cancer survival. These factors were selected for construction of the nomogram. The C-index of the nomogram was 0.71 (95% CI, 0.65 to 0.77), and calibration of the nomogram showed good agreement between the 5-year predicted survival and the actual observation.

Conclusions: We developed a nomogram predicting 5-year overall survival of surgically treated stage IA-IIB cervical cancer patients. More comprehensive information that is provided by this nomogram could provide further insight into personalized therapy selection.
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http://dx.doi.org/10.7314/apjcp.2015.16.9.3773DOI Listing
February 2016

Levels of polychlorinated biphenyls in settled house dust from urban dwellings in China and their neurodevelopmental effects on preschool-aged children.

Sci Total Environ 2015 Feb 21;505:402-8. Epub 2014 Oct 21.

Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China. Electronic address:

We investigated the levels of polychlorinated biphenyls (PCBs) in settled house dust (SHD) from urban dwellings with resident preschool-aged children in Nanjing, China. The possible neurodevelopmental effects of house-dust PCBs were also explored. SHD was collected from 114 urban houses. The levels of 39 PCB congeners were measured by gas chromatography-tandem mass spectrometry. The Child Behavior Checklist and the Gesell Development Inventory were used to evaluate the child's development. All 39 target congeners measured were detected. The mass percentage of di-PCBs was the highest at 47.8%, followed by tetra- and tri-PCBs at 16.8% and 13.0%, respectively. Spearman's rho correlation showed that di-, tri-, hexa-, hepta-, nona- and total PCBs were positively associated with somatic, thought problem and total problem scores (0.24
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http://dx.doi.org/10.1016/j.scitotenv.2014.10.026DOI Listing
February 2015

Levels of polybrominated diphenyl ethers in settled house dust from urban dwellings with resident preschool-aged children in Nanjing, China.

Arch Environ Contam Toxicol 2015 Jan 18;68(1):9-19. Epub 2014 Jul 18.

Qingdao Centers for Disease Control and Prevention, No. 175 Shandong Rd, Qingdao, 266033, China,

We investigated the levels and possible determinants of polybrominated diphenyl ethers (PBDEs) in the settled house-dust (SHD) of urban dwellings with resident preschool-aged children in Nanjing, China. The possible neurodevelopmental effects of house-dust PBDEs were also explored. SHD was collected from 216 urban houses. Levels of 8 PBDEs were measured by gas chromatography-negative chemical ionization mass spectrometry. The Child Behavior Checklist and the Gesell Development Inventory were used to evaluate the child's development. BDE47, BDE99, BDE153, BDE18, and BDE209 were detected in the SHD of >90 % of houses, of which BDE209 predominated. Most PBDEs were found at significantly greater levels in indoor than in outdoor dust (P < 0.05). Levels of BDE28 and BDE154 in houses with solid-wood floors were significantly greater than those in houses with plywood floors (P < 0.05). BDE154 levels in houses with wallpaper were significantly greater than those without wallpaper (P < 0.05). Greater BDE47 concentrations were found in houses with less natural ventilation time (linear trend P < 0.05). After dichotomization at the geometric mean concentration, BDE209 and total BDEs showed significant risks for depressed behavior problems and lower personal social developmental quotients (DQs); BDE99 and BDE153 indicated a risk for lower personal social DQs. In conclusion, PBDEs (especially BDE209) are ubiquitous in urban SHD in Nanjing residences. Natural ventilation and floor materials potentially influence PBDE levels in SHD. The potential adverse effect of postnatal exposure to PBDEs on the behavior and neurodevelopment of preschool-age children requires follow-up in larger studies.
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http://dx.doi.org/10.1007/s00244-014-0065-zDOI Listing
January 2015

Olmesartan medoxomil reverses glomerulosclerosis in renal tissue induced by myocardial infarction without changes in renal function.

Exp Ther Med 2014 Jul 25;8(1):105-109. Epub 2014 Apr 25.

Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning 110001, P.R. China.

The aim of the present study was to investigate the effect of olmesartan medoxomil (OLM) on renal injury in mice with myocardial infarction (MI). A total of 33 male C57/BL/6 mice were divided into a sham surgery group (SHAM group), MI group (MI group) and OLM treatment group (OLM group). Experimental MI models were established in the mice of the MI and OLM groups by coronary artery ligation, and the mice in the OLM group were fed a daily dose of 10 mg/kg OLM for eight weeks. The results showed that MI induced a reduction in cardiac function and an increase in systolic blood pressure. In addition, increased periodic acid-Schiff (PAS) positive staining, combined with increased levels of angiotensin II (Ang II) in the plasma and kidneys, and increased expression levels of renin, angiotensin II type 1 receptor (AT1R) and angiotensinogen (AGT) in the kidney tissues was observed compared with those in the SHAM group. OLM treatment attenuated the injury by reducing the systolic blood pressure and PAS positive staining, and decreasing the expression levels of Ang II, renin, AT1R and AGT in the kidney compared with those in the MI group. It may be concluded that MI activates the intrarenal renin-angiotensin system and leads to glomerulosclerosis, and that OLM protects the kidney by inhibiting the effects of Ang II.
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http://dx.doi.org/10.3892/etm.2014.1695DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061226PMC
July 2014

[Investigation on role of p38α mitogen-activated protein kinases in human esophageal squamous cell carcinoma cell line Eca109].

Zhonghua Yu Fang Yi Xue Za Zhi 2013 Aug;47(8):757-61

The First Affiliated Hospital of Xinjiang Medical University, State Key Lab Breeding Base of Xinjiang Major Disease Research, Urumqi 830011, China.

Objective: To investigate the role of p38α mitogen-activated protein kinases (MAPK) in human esophageal squamous cell carcinoma cell line Eca109.

Methods: Specific short hairpin (shRNA) vector as well as eukaryotic expression vector harbouring full length cDNA of human p38α MAPK were transfected into Eca109 cells. Cell proliferation after transfection was detected by MTT, cell cycle and apoptosis were assayed by flow cytometry. The variation of migration and invasion after transfection was determined using wound healing assay and Transwell assay, respectively.

Results: The proliferation of Eca109 cells after knock-down for 48 h (0.951 ± 0.086) was significantly increased (t = 3.20, P < 0.05) compared with control (0.811 ± 0.012), Sphase was increased but not significantly. Cell apoptosis rate after knock down for 48 h (17.400 ± 5.495) was significantly increased (t = 40.06, P < 0.01) compared with control(1.000 ± 0.721) . Migration after knock down for 72 h (0.034 ± 0.031) were enhanced pronouncedly (t = -5.79, P < 0.01) compared with control (0.278 ± 0.021) and invasive ability also increased; whereas the proliferation of Eca109 cells after over-expression for 48 h (0.472 ± 0.089) was inhibited significantly (t = -7.50, P < 0.01) compared with control(0.811 ± 0.012), cells arrested at G1 phase (t = 4.80, P < 0.01). Cell apoptosis rate (32.233 ± 1.457) were decreased significantly (t = 17.20, P < 0.01) compared with control (1.000 ± 0.721) mm, migration after overexpression for 72 h ((0.770 ± 0.054) mm) was suppressed pronouncedly compared with control groups of (0.278 ± 0.021) mm(t = 11.00, P < 0.01).Invasion after overexpression was inhibited.

Conclusions: p38α MAPK plays an anti-oncogenic role in the pathogenesis of esophageal squamous cell carcinoma cell line Eca109.
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August 2013

Role of neuronal nitric oxide synthase in the cardiac ischemia reperfusion in mice.

Chin J Physiol 2013 Oct 31;56(5):291-7. Epub 2013 Aug 31.

Department of Pathophysiology, College of Basic Medical Sciences, China Medical University Shenyang 110001, Liaoning, People's Republic of China.

Several studies have demonstrated the role of endothelial and inducible nitric oxide synthase in cardiac ischemia reperfusion(IR). However, the role of neuronal nitric oxide synthase (nNOS) in IR is still controversial. The present study was designed to explore the possible involvement of nNOS in cardiac IR. nNOS-/- knockout (KO) and wild type C57 (WT) mice were subjected to 45 min of ischemia by left descending branch of coronary artery ligation followed by 3 h reperfusion, which plasma was collected for creatine kinase (CK) and lactate dehydrogenase (LDH) measurements, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and measurements of activities of caspase-3, -8, -9, phospho-p38, -ERK, -JNK mitogen-activated protein kinase (MAPK) and phospho-nNOS, phospho-eNOS and iNOS. IR induced cardiac tissue apoptosis by increases of TUNEL staining and activities of caspase-3, -8, and -9, accompanied with increase of CK and LDH concentration and phosphorylation of p38, ERK and JNK MAPK and phospho-nNOS, phospho-eNOS and iNOS in both mouse strains. However, IR induced increases of TUNEL staining and activities of caspase-3, -8 and -9, and CK and LDH concentrations and activation of p38 MAPK were markedly lower in KO mice compared with WT mice. But the phosphorylation of eNOS was significantly higher compared with WT IR group (P < 0.05). The data obtained suggest that nNOS exacerbates IR-induced injury maybe involving p38 MAPK activation.
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http://dx.doi.org/10.4077/CJP.2013.BAB143DOI Listing
October 2013

A high-fat diet induces obesity and impairs bone acquisition in young male mice.

Mol Med Rep 2013 Apr 29;7(4):1203-8. Epub 2013 Jan 29.

Department of Pathophysiology, College of Basic Medicine, China Medical University, Shenyang, Liaoning 110001, P.R. China.

The postnatal development of obesity is highly associated with the excessive consumption of a high-calorie, high-fat diet (HFD). However, the correlation between HFD-induced pediatric obesity and skeletal development remains to be elucidated. In the present study, postnatal day 17 (PND17) mice were weaned on a HFD for eight weeks ad libitum to induce obesity. The HFD mice showed a significant increase in the total body weight and gonadal and abdominal fat mass compared with the control animals. Peripheral quantitative (pQ) CT scans of the tibial bone revealed that the bone mineral density (BMD), including the total, trabecular and cortical BMD, was unchanged between the HFD and control diet groups, but that it was inversely associated with body fat. By contrast, the bone mineral content (BMC) and trabecular area were significantly decreased in the HFD group compared with the control. RNA and protein were isolated from the femur. qPCR and western blot analyses showed a significant downregulation in the gene expression of the key canonical Wnt signaling molecule β-catenin, the osteoblastic cell differentiation marker Runt-related transcription factor 2 (Runx2) and also in the β-catenin gene encoded protein levels of the HFD mice when compared with the controls. Consistent with the increased fat mass in the HFD-induced obese animals, the expression of the adipogenic genes and aP2 was increased compared with the controls. Bone marrow cells were aspirated and the ex vivo bone marrow cell cultures showed that the number of colony-forming unit osteoblasts (CFU-OBs) per bone was significantly decreased in the samples from the HFD mice compared with those from the controls. These observations suggested that HFD-induced obesity in growing animals may affect the total available osteoblastic cell differentiation progenitors in the bone, while increasing adipogenesis. This may result in negative consequences for the bone later on in adult life.
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http://dx.doi.org/10.3892/mmr.2013.1297DOI Listing
April 2013

A modified triple incision technique for women with locally advanced vulvar cancer: a description of the technique and outcomes.

Eur J Obstet Gynecol Reprod Biol 2012 Oct 26;164(2):185-90. Epub 2012 Jun 26.

Department of Gynaecologic Oncology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, PR China.

Objective: Women with locally advanced vulvar carcinoma have an excellent chance of a cure by undergoing a radical vulvectomy with an "en bloc" inguinofemoral lymphadenectomy, but the morbidity associated this surgical approach is substantial. To achieve an outcome comparable with the traditional radical method in terms of oncologic safety, and an improved post-operative quality of life, we modified the classic triple-incision technique and suggested it as an alternative for these patients. The aim of this study was to report this new technique.

Study Design: Between January 2004 and November 2009, 24 patients with clinical stage T2 (≥ 4 cm) or T3 invasive vulvar cancer underwent surgical treatment with our modified triple incision technique. Their clinical and surgical complications and follow-up data were retrospectively reviewed.

Results: The post-surgical complications were as follows: lymphoedema in 45.8%, wound breakdown in 20.8% and cellulitis in 8.3%. After a median follow-up of 35.5 months, three (12.5%) patients developed a recurrence in the skin bridge (2/24, 8.3%) or lungs (1/24, 4.2%). All patients suffering from skin bridge recurrences were salvaged by local re-resection. Four (16.7%) cases of death were noted: three (12.5%) patients died of non-cancer-related diseases and one (4.2%) died from a multifocal pulmonary metastasis; no evidence of vulvar or groin disease was observed at these patients' last follow-up.

Conclusion: The modified triple-incision technique described in this preliminary study appears to be safe, feasible and tolerable for patients with a locally advanced vulvar cancer, and offers an acceptable morbidity.
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http://dx.doi.org/10.1016/j.ejogrb.2012.05.035DOI Listing
October 2012

An effective and safe supplement for stem cells expansion ex vivo: cord blood serum.

Cell Transplant 2012 13;21(5):857-69. Epub 2011 Dec 13.

Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang, China.

Mesenchymal stem cells (MSCs) are potential and optimal stem cells in clinical cell therapy, and fetal bovine serum (FBS) is widely used for expansion of MSCs, despite the risks of infectious disease transmission and immunological reaction of the xenogenic origin. This study was designed to compare human four blood group cord blood serum (CBS) with FBS in culturing human placenta-derived mesenchymal stem cells (hPDMSCs), which were derived from four blood group donors. The expansion medium included: 10% FBS, 10% A-CBS, 10% B-CBS, 10% O-CBS, and 10% AB-CBS. Cumulative population doubling, generation time, fold expansion rates and differentiation capacity, cell cycle, and immunophenotype were also assessed. The results showed that fold expansion rate and cumulative population doubling of hPDMSCs significantly increased during long-term MSC expansion in CBS medium, but the generation time decreased compared with FBS. CBS might be an effective supplement for stem cells expand rapidly ex vivo. Cell cycle and differentiation assays showed that most of the hPDMSCs expanding in the presence of CBS were in stationary phase, which was the characteristic of stem cells, and they retained their ability to differentiate into chondrogenic and endothelial cells. By comparing these four blood groups of CBS, we found that there was no significant difference among different blood groups in culturing hPDMSCs, which were isolated from different blood group donors. So CBS may be an optimal replacement to avoid the risks of FBS application in expansion of stem cell for clinical cell therapy and tissue engineering.
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http://dx.doi.org/10.3727/096368911X612486DOI Listing
November 2012

The status of phosphorylated p38 in esophageal squamous cell carcinoma.

Mol Biol Rep 2012 May 14;39(5):5315-21. Epub 2011 Dec 14.

Medical Research Center, The Affiliated Hospital, Xinjiang Medical University, Urumqi, 830054, Xinjiang Uygur Autonomous Region, People's Republic of China.

The p38 mitogen-activated protein kinase (MAPK) is a member of the MAPK family, which is initially found to be activated by stress stimuli, proinflammatory cytokines, and growth factors. However, its role in the pathogenesis of esophageal squamous cell carcinoma (ESCC) is largely unkown, so we investigate the role of phosphorylated p38 (p-p38) MAPK in ESCC. First of all, in vitro cell line ECa109, SB203580 as selective inhibitor of p38, can suppress the growth of esophageal cancer cell in a dose- and time-dependent way, suggesting that ECa109 cell growth and proliferation was closely associated with p-p38. Using western-blot analysis of fresh 16 paired surgically resected ESCC and matched non-tumor adjacent tissues (NAT), we showed that p-p38 was significantly expressed higher in NAT compared to ESCC. Moreover, expressions of p-p38 were further confirmed by 162 paired of formalin-fixed paraffin-embedded (FFPE) ESCC and NAT by immunohistochemistry, the same trend result was obtained through statistical analysis that there was increased expression of p-p38 in NAT as compared with ESCC (P < 0.01), and expression of p-p38 was not significantly associated with lymph nodes metastasis (P > 0.05) and ESCC differentiation degree (P > 0.05). Taken together, all the results we obtained demonstrated that p-p38 plays a key role in the malignant transformation of ESCC.
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http://dx.doi.org/10.1007/s11033-011-1330-0DOI Listing
May 2012

[Expression of ERK1/2 MAPK signaling transduction pathway in esophageal cancers in Kazakh patients].

Zhonghua Zhong Liu Za Zhi 2011 Jun;33(6):421-5

Medical Research Center, First Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, China.

Objective: To investigate the expression variation and significance of ERK1/2 MAPK signaling transduction pathway in the pathogenesis of esophageal squamous cell carcinoma (ESCC) in Kazakh patients.

Methods: The expression level of p-ERK1/2 after serum starvation and treatment with U0126 inhibitor was detected in esophageal cancer cell line EC9706 by Western blot assay. The mRNA level of total ERK1/2 (t-ERK1/2) and expression level of t-ERK1/2 and p-ERK1/2 proteins of 25 pairs of ESCC and adjacent normal esophageal mucosal tissues of Kazakh patients were examined and identified by real-time quantitative PCR (qRT-PCR) and Western blotting, respectively. The expression of p-ERK1/2 protein was verified by immunohistochemistry in 126 paraffin-embeded specimens, including 19 normal esophageal mucosa, 55 esophageal carcinomas in situ and 52 invasive carcinomas.

Results: ERK1/2 MAPK signaling transduction pathway was in an active status in the EC9706 cells. The expression level of p-ERK1/2 in Ec9706 cells reached a peak at 10 min after transient serum stimulation, and p-ERK1/2 expression was totally restrained after the treatment with 50 µmol/L U0126. In the 25 pairs of ESCC and adjacent normal mucosa, the t-ERK1 mRNA level was 1.92 ± 3.49 in the ESCC tissues and 3.67 ± 7.47 in the adjacent normal mucosa. The t-ERK1 mRNA level in ESCC tissues was significantly lower than that in adjacent normal mucosa (P < 0.05), whereas there was no significant difference of t-ERK2 mRNA level between them(P > 0.05). The expression levels of p-ERK1 and p-ERK2 proteins were 0.87 ± 0.14 and 0.79 ± 0.10 in the ESCC tissues, and 1.10 ± 0.13 and 1.32 ± 0.12 in the adjacent normal mucosae. p-ERK1/2 protein in the ESCC tissues was significantly lower than that in the adjacent normal tissue (P < 0.01). However, there was no significant difference between their t-ERK1/2 protein levels (P > 0.05). In the 126 cases of paraffin-embeded specimens, positive expressions of both p-ERK1 and p-ERK2 in esophageal cancer tissues were 7.7% (4/52), significantly lower than those in adjacent normal mucosa (31.6%, 6/19) and carcinoma in situ (85.5%, 47/55, P < 0.05).

Conclusions: ERK1/2 MAPK signaling pathway is in an active status in esophageal cancer and adjacent normal mucosa. Our results imply that the activation of p-ERK1/2 MAPK signaling transduction pathway plays a role in the early pathogenesis of ESCC in Kazakh patients.
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June 2011

Clinicopathological pattern and Annexin A2 and Cdc42 status in patients presenting with differentiation and lymphnode metastasis of esophageal squamous cell carcinomas.

Mol Biol Rep 2012 Feb 21;39(2):1267-74. Epub 2011 May 21.

Medical Research Center, The Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, People's Republic of China.

Annexin A2 and Cdc42 were identified by 2-dimensional electrophoresis (2-DE) and MALDI-TOF-MS between esophageal squamous cell carcinomas (ESCC) and corresponding normal esophagus mucosa in our previous study. To assess clinico-pathological pattern and Annexin A2 and Cdc42 status with respect to cell differentiation and lymphnode metastasis in patients with ESCC. The expression of Annexin A2 and Cdc42 in 22 pairs of fresh ESCC and matched tissues were detected by qRT-PCR and western blot, respectively. And it was further confirmed by immunohistochemistry with 175 pairs of formalin-fixed, paraffin-embedded ESCC. Results showed that Annexin A2 expression was significantly down-regulated, and Cdc42 was up-regulated in ESCC compared to matched control on both mRNA and protein level (P < 0.05), which was in accordance with our previous results on proteomics data. Additionally, Annexin A2 and Cdc42 expression was significantly correlated with lymphoid node metastasis (P < 0.05) and pathological differentiation (P < 0.05). Taken together, we proposed that the aberrant expression of Annexin A2 and Cdc42 played a role in carcinogenesis, differentiation and metastasis of ESCC, which implied its potential target for clinical biomarkers in differentiation and lymph node metastasis.
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http://dx.doi.org/10.1007/s11033-011-0859-2DOI Listing
February 2012

Role of microRNA let-7 and effect to HMGA2 in esophageal squamous cell carcinoma.

Mol Biol Rep 2012 Feb 20;39(2):1239-46. Epub 2011 May 20.

Medical Research Center, the Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, People's Republic of China.

To investigated the role of microRNA (miRNA) let-7 and its regulation on high mobility group A2 (HMGA2) protein expression in esophageal squamous cell carcinoma (ESCC). Let-7 expressions were detected in esophageal cancer cell line Eca109, and 45 paired of fresh ESCC and normal adjacent tissues (NAT) by real-time quantitative PCR (qRT-PCR). To evaluate the role of let-7 and HMGA2, cell proliferations were analyzed with synthetic let-7 mimics- or its inhibitor-transfected cells. Moreover, expressions of HMGA2 were performed by western blotting and further confirmed by 150 paired of formalin-fixed, paraffin-embeded (FFPE) ESCC and NAT by immunohistochemistry (IHC). In Eca109, when transfected with let-7 mimics, accumulation of let-7 was obviously suppressed cell proliferation with approximately 14%. Conversely, when Eca109 transfected with let-7 inhibitor, expression of let-7 was declined, which promoted cell proliferation with approximately 16%. Both of them had no effect on the level of HMGA2 mRNA. The transcription of let-7 inversely correlated with HMGA2 protein. Compared with the NAT, expression of let-7 was significantly lower in ESCC tissues (P < 0.05), and there was a significant correlation between low expression of let-7 and lymph node metastasis in ESCC (P < 0.05). Moreover, the protein expression of HMGA2 was significantly higher in ESCC compared with NAT (P < 0.05). However, mRNA expression of HMGA2 had no obvious significance between them. The present results demonstrated that let-7 and HMGA2 involved in ESCC carcinogenesis. Let-7 could inhibit cell proliferation and lower expressed in ESCC, and there was a correlation between let-7 lower expression and lymph node metastasis in ESCC patients. As well as, HMGA2 protein expression was significantly higher in ESCC than that in NAT, and HMGA2 may negatively regulated by let-7 at the post- transcriptional level in ESCC.
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http://dx.doi.org/10.1007/s11033-011-0854-7DOI Listing
February 2012

Analysis of XPD genetic polymorphisms of esophageal squamous cell carcinoma in a population of Yili Prefecture, in Xinjiang, China.

Mol Biol Rep 2012 Jan 7;39(1):709-14. Epub 2011 May 7.

Medical Research Center, the First Affiliated Hospital, Xinjiang Uygur Autonomous Region, Xinjiang Medical University, Urumqi, 830054, People's Republic of China.

To evaluate the association with genetic polymorphisms in Xeroderma pigmentosum complementation group D (XPD) gene of esophageal squamous cell carcinoma (ESCC) risk in a population of Yili Prefecture, in Xinjiang, China. A hospital-based case-control study was designed with 571 samples including 213 ESCC patients and 358 controls with age, gender and ethnicity-matched subjects (Kazakh, Uygur and Han ethnic). Genotypes were determined by PCR restriction fragment length polymorphism (PCR-RLFP) and confirmed by sequence. Relative risk associated with a particular genotype was estimated by calculating odds ratios (OR) along with 95% confidence intervals (CI). Significant ESCC risk was observed for XPD Lys751Gln (rs13181) frequency of presence C allele (OR: 1.409, 95% CI: 1.005-1.976) in the three ethnics. XPD Asp312Asn (rs1799793) of Han ethnic was associated with a borderline decrease of ESCC (OR: 0.362, 95% CI: 0.145-0.906), however, it was associated with ESCC risk in Uygur ethnic (OR: 2.403, 95% CI: 1.087-5.310). The results demonstrated an association between the XPD Lys751Gln (rs13181) for frequency of presence C allele and risk for ESCC in the three ethnics of Yili Prefecture, in Xinjiang, China. XPD Asp312Asn (rs1799793), which was associated with a borderline decrease of Han ethnic and risk of Uygur ethnic of ESCC, may play a different role in the three ethnics of ESCC.
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http://dx.doi.org/10.1007/s11033-011-0789-zDOI Listing
January 2012

Proteomic identification of differentially-expressed proteins in esophageal cancer in three ethnic groups in Xinjiang.

Mol Biol Rep 2011 Jun 2;38(5):3261-9. Epub 2010 Dec 2.

Medical Research Center, the First Affiliated Hospital, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830054, People's Republic of China.

The Objective is to identify candidate biomarkers for Squamous cell carcinoma (ESCC) in three ethnics in Xinjiang as well as reveal molecular mechanism. Proteins from 15 pairs of ESCC and matching adjacent normal esophageal tissues (five pairs in each ethnic of Kazakh, Uygur and Han) were separated by 2-DE and differentially proteins were identified by matrix-assisted laser desorption/ionization time-of-flight MS. After identified by Mascot database, some of interesting proteins were confirmed in the other 175 pairs of ESCC by immuno histochemistry. Comparison of patterns revealed 20 proteins significantly changed, of which 12 protein with concordantly increased, such as ACTB protein, COMT protein, Syntaxin binding protein Pyruvate Kinase (PKM2), Cathepsin D, Chromosome 1 open reading frame 8, Heat shock protein 27, Cdc42, Proteosome, LLDBP, Immunoglobulin, TNF receptor associated factor 7; and eight protein spots with concordantly decreased intensity in ESCC, such as Adenylate kinase 1, General transcription factor II H, Smooth muscle protein, Trangelin, Early endosome antigen 1, Annexin A2, Fibrin beta, Tropomyosin. There were a significant difference in protein overexpression of PKM2 (74.9%) and Cathepsin D (85.1%) in ESCC compared to adjacent tissues (P < 0.05) by immunohistochemistry. Further, overexpression of Cathepsin D was obvious difference in Hazakh ESCC (94.7%) than that in Uygur (78.6%) (P < 0.05). Interestingly, the overexpression of Cathepsin D was reversely associated with ESCC differentiation (P < 0.05). Twenty proteins differentially-expressed between ESCC and normal tissues were identified. Cathepsin D and PKM2 were for the first time observed to be dysregulated in Kazakh's ESCC. Moreover, Cathepsin D may play a complicated role both in carcinogenesis and cell-differentiation of ESCC.
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http://dx.doi.org/10.1007/s11033-010-0586-0DOI Listing
June 2011

Role of microRNA-21 and effect on PTEN in Kazakh's esophageal squamous cell carcinoma.

Mol Biol Rep 2011 Jun 20;38(5):3253-60. Epub 2010 Nov 20.

Medical Research Center, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, 830054 Xinjiang Uygur Autonomous Region, People's Republic of China.

The aim of this study was investigate the role of microRNA-21 (miR-21) and its regulation on phosphatase and tensin homolog deleted from chromosome-10 (PTEN) in Kazakh's esophageal squamous cell carcinoma (ESCC). MiR-21 expressions were investigated in esophageal cancer cell line Eca109, and 18 pairs of Kazakh's ESCC and adjacent normal tissues by real-time quantitative PCR (qRT-PCR). To evaluate the role of miR-21 and PTEN, cell proliferations were analyzed with miR-21 mimics or their inhibitor-transfected cells. Moreover, the expressions of PTEN were performed by Western blotting. In Eca109, when transfected with miR-21 mimics, accumulation of miR-21 was obviously increased and expression of PTEN protein was decreased to be approximately 40%, which resulted in the promotion of cell proliferation. However, when transfected with miR-21 inhibitor, expression of miR-21 was declined and PTEN protein was overexpressed to be approximately 79%, which resulted in the suppression of cell proliferation. Both of them had no effect on the level of PTEN mRNA. Compared with adjacent normal tissues, miR-21 expression was significantly higher in tumor (P < 0.05). Specifically, patients with cancer cell invasion deep into esophageal serosa showed significantly higher expression of miR-21. Protein expression of PTEN was significantly lower in tumor compared with normal tissues (P < 0.05); however, mRNA expression of PTEN had no obvious significance between them. Furthermore, there was a significantly inverse correlation between miR-21 expression and PTEN protein levels (p < 0.05). The author concluded that MiR-21 was overexpressed in vitro and ESCC, and promoted the cell proliferation, might target PTEN at post-transcriptional level, and regulated the cancer invasion in Kazakh's ESCC.
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http://dx.doi.org/10.1007/s11033-010-0480-9DOI Listing
June 2011

Polymorphisms of COMT and XPD and risk of esophageal squamous cell carcinoma in a population of Yili Prefecture, in Xinjiang, China.

Biomarkers 2011 Feb 27;16(1):37-41. Epub 2010 Oct 27.

Medical Research Center, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang Uygur, PR China.

Objective: To investigate polymorphisms of COMT (Rs4680) and XPD (Rs13181) and risk of esophageal squamous cell carcinoma (ESCC) in a population from Yili Prefecture, Xinjiang, China.

Methods: A hospital-based case-control study was designed. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Odds ratios (OR) and 95% confidence intervals (CI) were analysed using unconditional logistic regression.

Results: An increased risk of ESCC was discovered with COMT in relation to the frequency of the presence of the A allele (Rs4680; OR 1.30, 95% CI 1.00-1.68). An individual with combined COMT 158 (Val/Met or Met/Met) and XPD 751 (Lys/Gln or Gln/Gln) genotype had an increased ESCC risk.

Conclusions: Polymorphic variation in COMT Val158Met and XPD Lys751Gln may be important for ESCC susceptibility.
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http://dx.doi.org/10.3109/1354750X.2010.522732DOI Listing
February 2011

Simple conjugated polymers with on-chain phosphorescent iridium(III) complexes: toward ratiometric chemodosimeters for detecting trace amounts of mercury(II).

Chemistry 2010 Oct;16(40):12158-67

Key Laboratory for Organic Electronics & Information Displays (KLOEID) and Institute of Advanced Materials (IAM), Nanjing University of Posts & Telecommunications (NUPT), 9 Wenyuan Road, Nanjing 210046, P.R. China.

For the development of excellent optical probes for mercury(II), a series of simple conjugated polymers that contain phosphorescent iridium(III) complexes as receptors for mercury(II) were designed and synthesized. These conjugated polymers showed energy transfer from the polymer host to iridium(III) complex guest in both solution and the solid state. Unexpectedly, they can work as excellent polymer chemodosimeters for mercury(II) by utilizing the mercury(II)-induced decomposition of iridium(III) complex. They exhibit a pronounced optical signal change with switchable phosphorescence and fluorescence, even when the concentration of a solution of mercury(II) in THF was as low as 0.5 ppb. With the addition of mercury(II), the phosphorescent emission intensity of iridium(III) complexes was quenched completely. As the emission from polymer backbones increased, the emission wavelength was redshifted simultaneously, thereby realizing ratiometric detection. Excellent selectivity toward mercury(II) over other potentially interfering cations was also realized. In addition, an obvious emission color change of polymer solution from red to yellow-green was observed, thus realizing a "naked-eye" detection of mercury(II). More importantly, the solid films of these polymer chemodosimeters also exhibited high sensitivity and rapid response to mercury(II), thereby demonstrating the possibility of the fabrication of sensing devices with fast and convenient detection of mercury(II). The sensing mechanism was also investigated in detail. This is the first report on chemodosimeters based on conjugated polymers with phosphorescent iridium(III) complexes.
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http://dx.doi.org/10.1002/chem.201000748DOI Listing
October 2010

Genome-wide association study of esophageal squamous cell carcinoma in Chinese subjects identifies susceptibility loci at PLCE1 and C20orf54.

Nat Genet 2010 Sep 22;42(9):759-63. Epub 2010 Aug 22.

Cancer Research Center, Xinxiang Medical University, Xinxiang, Henan, China.

We performed a genome-wide association study of esophageal squamous cell carcinoma (ESCC) by genotyping 1,077 individuals with ESCC and 1,733 control subjects of Chinese Han descent. We selected 18 promising SNPs for replication in an additional 7,673 cases of ESCC and 11,013 control subjects of Chinese Han descent and 303 cases of ESCC and 537 control subjects of Chinese Uygur-Kazakh descent. We identified two previously unknown susceptibility loci for ESCC: PLCE1 at 10q23 (P(Han combined for ESCC) = 7.46 x 10(-56), odds ratio (OR) = 1.43; P(Uygur-Kazakh for ESCC) = 5.70 x 10(-4), OR = 1.53) and C20orf54 at 20p13 (P(Han combined for ESCC) = 1.21 x 10(-11), OR = 0.86; P(Uygur-Kazakh for ESCC) = 7.88 x 10(-3), OR = 0.66). We also confirmed association in 2,766 cases of gastric cardia adenocarcinoma cases and the same 11,013 control subjects (PLCE1, P(Han for GCA) = 1.74 x 10(-39), OR = 1.55 and C20orf54, P(Han for GCA) = 3.02 x 10(-3), OR = 0.91). PLCE1 and C20orf54 have important biological implications for both ESCC and GCA. PLCE1 might regulate cell growth, differentiation, apoptosis and angiogenesis. C20orf54 is responsible for transporting riboflavin, and deficiency of riboflavin has been documented as a risk factor for ESCC and GCA.
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http://dx.doi.org/10.1038/ng.648DOI Listing
September 2010

The expression and activation of ERK/MAPK pathway in human esophageal cancer cell line EC9706.

Mol Biol Rep 2011 Feb 13;38(2):865-72. Epub 2010 May 13.

Medical Research Center, the First Affiliated Hospital, Xinjiang Medical University, Urumqi, 830054, Xinjiang Uygur Autonomous Region, People's Republic of China.

While there have been more and more studies concerning mitogen-activated protein kinases (MAPKs) signaling pathways, which control many cellular complex programmes, such as cell proliferation, differentiation, cell death and embryogenesis. However, few studies are carried out about expression and activation of classical MAPKs, extracellular signal-regulated kinase1/2 (ERK1/2) in human esophageal cancer cell line. Therefore, in the present study, we investigated the expression and activation of ERK1/2 in human esophageal cancer cell line EC9706 and human normal esophageal epithelial cell line Heepic, which is as control. This study showed that ERK1/2 was transiently phosphorylated both in EC9706 and Heepic, the kinetics of which were slightly different. To further study the ERK/MAPK signaling pathway in EC9706 and Heepic cell line, U0126 a kind of specific inhibitor of MEK was used. This study showed that U0126 can block the phosphorylation of ERK1/2 in a short time, the complete inhibition concentration for EC9706 and Heepic cell line is 50 and 20 μM, respectively. Incidentally, to further investigate the different roles of ERK1 and ERK2, vector-based short hairpin interference vectors targeted on ERK1/2 was constructed. Moreover, the effective interference target sequence was screened out in a transient transfection manner. MTT experiment showed that ERK2 is more important than ERK1 in the proliferation of EC9706 cells.
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http://dx.doi.org/10.1007/s11033-010-0178-zDOI Listing
February 2011

shRNA interference for extracellular signal-regulated kinase 2 can inhibit the growth of esophageal cancer cell line Eca109.

J Recept Signal Transduct Res 2010 Jun;30(3):170-7

Medical Research Center, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region, China.

Background: Esophageal squamous cell carcinoma is one of the most common digestive tract cancers with 5-year survival rate less than 10% owing to its poor prognosis. Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway has been mainly involved in the pathogenesis of various cancers. In present study, we investigated the role of ERK2 in human esophageal cancer cell line Eca109.

Methods: Short-hairpin RNA (shRNA) interference vector targeted ERK2 was constructed using pGeneclip U1 hairpin cloning systems, then transfected into Eca109 cell line. The transfection efficiency was observed by fluorescence microscope and cell growth after transfection with shRNA-ERK2 vector was determined by methylthiazolyl blue tetrazolium (MTT) assay. The ERK2 expression after transfection was detected by western-blotting. The cell apoptosis and cell-cycle was analyzed by flow cytometry. The role of p-ERK2 was confirmed by immunohistochemistry and soft agar colony formation assay.

Results: The growth of Eca109 transfected with shRNA-ERK2 vector was obviously inhibited compared to control group via MTT analysis. The inhibition rate after transfection with shRNA-ERK2 for 96 h was 10.45%, the expression of ERK2 was obviously reduced compared to the control analyzed by western-blot, cell apoptosis was 9.7% (compared to control, P < 0.05), and cell-cycle was arrested at G1 phase.

Conclusions: In present study we demonstrated for the first time that transfection with shRNA-ERK2 targeted ERK2 into Eca109 cells can inhibit growth of Eca109, inducing cell apoptosis and influencing cell-cycle. Together, these results we obtained suggested that ERK2 plays an important role in cell growth of Eca109.
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http://dx.doi.org/10.3109/10799891003786200DOI Listing
June 2010

DNA polymorphism and risk of esophageal squamous cell carcinoma in a population of North Xinjiang, China.

World J Gastroenterol 2010 Feb;16(5):641-7

Medical Research Center, the First Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China.

Aim: To investigate the role of metabolic enzyme and DNA repair genes in susceptibility of esophageal squamous cell carcinoma (ESCC).

Methods: A case-control study was designed with 454 samples from 128 ESCC patients and 326 gender, age and ethnicity-matched control subjects. Genotypes of 69 single nucleotide polymorphisms (SNPs) of metabolic enzyme (aldehyde dehydrogenase-2, ALDH2; alcohol dehydrogenase-1 B, ADHB1; Cytochrome P450 2A6, CYP2A6) and DNA repair capacity genes (excision repair cross complementing group 1, ERCC1; O(6)-methylguanine DNA methyltransferase, MGMT; xeroderma pigmentosum group A, XPA; xeroderma pigmentosum group A, XPD) were determined by the Sequenom MassARRAY system, and results were analyzed using unconditional logistic regression adjusted for age, gender.

Results: There was no association between the variation in the ERCC1, XPA, ADHB1 genes and ESCC risk. Increased risk of ESCC was suggested in ALDH2 for frequency of presence C allele of SNP [Rs886205: 1.626 (1.158-2.284)], XPD for C allele [Rs50872: 1.482 (1.058-2.074)], and MGMT for A allele [Rs11016897: 1.666 (1.245-2.228)]. Five variants of MGMT were associated with a protective effect on ESCC carcinogenesis, including C allele [Rs7069143: 0.698 (0.518-0.939)], C allele [Rs3793909: 0.653 (0.429-0.995)], A allele [Rs12771882: 0.719 (0.524-0.986)], C allele [Rs551491: 0.707 (0.529-0.945)], and A allele [Rs7071825: 0.618 (0.506-0.910)]. At the genotype level, increased risk of ESCC carcinogenesis was found in homozygous carriers of the ALDH2 Rs886205 [CC vs TT, odds ratios (OR): 3.116, 95% CI: 1.179-8.234], MGMT Rs11016879 (AA vs GG, OR: 3.112, 95% CI: 1.565-6.181), Rs12771882 (AA vs GG, OR: 2.442, 95% CI: 1.204-4.595), and heterozygotes carriers of the ALDH2 Rs886205 (CT vs TT, OR: 3.930, 95% CI: 1.470-10.504), MGMT Rs11016879 (AG vs GG, OR: 3.933, 95% CI: 2.216-6.982) and Rs7075748 (CT vs CC, OR: 1.949, 95% CI: 1.134-3.350), respectively. Three variants were associated with a protective effect on ESCC carcinogenesis, carriers of the MGMT Rs11016878 (AG vs AA, OR: 0.388, 95% CI: 0.180-0.836), Rs7069143(CT vs CC, OR: 0.478, 95% CI: 0.303-0.754) and Rs7071825 (GG vs AA, OR: 0.493, 95% CI: 0.266-0.915). Increased risk of ESCC metastasis was indicated in MGMT for frequency of presence C allele [Rs7068306: 2.204 (1.244-3.906)], A allele [Rs10734088: 1.968 (1.111-3.484)] and C allele [Rs4751115: 2.178 (1.251-3.791)]. Two variants in frequency of presence C allele of CYP2A6 [Rs8192720: 0.290 (0.099-0.855)] and A allele of MGMT [Rs2053139: 0.511 (0.289-0.903)] were associated with a protective effect on ESCC progression. Increased risk of ESCC metastasis was found in heterozygote carriers of the MGMT Rs7068306 (CG vs CC, OR: 4.706, 95% CI: 1.872-11.833).

Conclusion: Polymorphic variation in ALDH2, XPD and MGMT genes may be of importance for ESCC susceptibility. Polymorphic variation in CYP2A6 and MGMT are associated with ESCC metastasis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2816280PMC
http://dx.doi.org/10.3748/wjg.v16.i5.641DOI Listing
February 2010

[Metabonomic variation of esophageal cancer within different ethnic groups in Xinjiang, China].

Zhonghua Yu Fang Yi Xue Za Zhi 2009 Jul;43(7):591-6

Department of Thoracic Surgery, the First Affiliated Hospital, Xinjiang Medical University, Urumqi, China.

Objective: To investigate the metabonomic variation between patients with esophageal cancer (EC) and healthy controls, and to analyze the variation between patients with EC.

Methods: H-MR and orthogonal partial least-squares discriminant analysis (OPLS-DA) was performed on 108 plasma specimens from EC patients and 50 health controls, and the metabonomic variation between patients with EC and healthy controls analyzed.

Results: OPLS-DA analysis might correctly separate all plasma specimens from health controls and patients with EC, leucine (0.0043 +/- 0.0006, 0.0040 +/- 0.0006), alanine (0.0039 +/- 0.0007, 0.0033 +/- 0.0006), isoleucine (0.0067 +/- 0.0010, 0.0063 +/- 0.0009), valine (0.0037 +/- 0.0005, 0.0035 +/- 0.0006), glycoprotein (0.0123 +/- 0.0043, 0.0102 +/- 0.0022), lactate (0.0342 +/- 0.0113, 0.0258 +/- 0.0085), acetone (0.0027 +/- 0.0023, 0.0017 +/- 0.0008), acetate (0.0007 +/- 0.0001, 0.0006 +/- 0.0001), choline (0.0035 +/- 0.0006, 0.0029 +/- 0.0007), isobutyrate (0.0020 +/- 0.0004, 0.0018 +/- 0.0003), unsaturated lipid (0.0072 +/- 0.0013, 0.0059 +/- 0.0018), VLDL (0.1209 +/- 0.0589, 0.0879 +/- 0.0269), LDL (0.0885 +/- 0.0328, 0.0785 +/- 0.0288), 1-methylhistidine (0.0005 +/- 0.0001, 0.0004 +/- 0.0005) decreased in EC patient' s plasma with statistical significance (r total > 0.27, P < 0.05), dimethylamine (0.0004 +/- 0.0001, 0.0005 +/- 0.0001), alpha-glucose (0.0079 +/- 0.0013, 0.0081 +/- 0.0016), 3-glucose (0.0139 +/- 0.0024, 0.0142 +/- 0.0029), citric acid (0.0044 +/- 0.0008, 0.0106 +/- 0.0058) increase in the EC patient's plasma (r total < -0.27, P < 0.05). There were clear variation between Han and Kazak patients, alanine (0.0031 +/- 0.0005,0.0029 +/- 0.0004), glutamine (0.0010 +/- 0.0001, 0.0009 +/- 0.0001), tyrosine (0.0009 +/- 0.0001, 0.0008 +/- 0.0001), 1-methylhistidine (0.0005 +/- 0.0001, 0.0004 +/- 0.0001) increased in the Han patients (r > 0.35, P> 0.05), carnitine (0.0028 +/- 0.0006) was higher in Kazak patients than in Han patients (0.0025 +/- 0.0004), which had statistical significance (r = - 0.40, P < 0.05). Unsaturated lipid (0.0059 +/- 0.0018, 0.0047 +/- 0.0011), isoleucine (0.0062 +/- 0.0011, 0.0058 +/- 0.0007), alanine (0. 0032 +/- 0.0007, 0.0028 +/- 0.0004), glycoprotein (0.0096 +/- 0.0019, 0.0086 +/- 0.0011), glutamine (0.0011 +/- 0.0001, 0.0009 +/- 0.0001), tyrosine (0.0009 +/- 0.0001, 0.0008 +/- 0.0001), 1-methylhistidine (0.0005 +/- 0.0001, 0.0004 +/- 0.0001) were increased in Uygur patients as compared with Kazak patients, having statistical significance (r > 0.33, P < 0.05), carnitine (0.0027 +/- 0.0005) was higher in Kazak patients than in Uygur patients (0.0025 +/- 0.0004) (r = - 0.36, P < 0.05).

Conclusion: The results indicate that 1H-MR spectra of plasma analyzed by OPLS-DA statistical methods might completely separate the EC patients from health controls. The metabonomic approach should be helpful in screening of EC patients.
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July 2009

[Influences of lymphatic vessel ligation in pelvic lymphadenectomy on postoperative lymphocyst formation--a randomized controlled trial].

Ai Zheng 2009 Nov;28(11):1193-7

Department of Gynecology and Obstetrics, The Second Affiliated Hospital, Sun Yat-sen University, Guangdong, P. R. China.

Background And Objective: Pelvic lymphocysts are the most common postoperative complications of pelvic lymphadenectomy. Prevention of this disease is more important than treatment. This randomized study was to evaluate the preventive effect of lymph vessel ligation during pelvic lymphadenectomy on pelvic lymphocyst formation.

Methods: A total of 39 patients with gynecologic malignancy, who had pelvic lymphadenectomy in the Second Affiliated Hospital of Sun Yat-sen University from July 2006 to January 2007, were randomized into the ligation group (19 patients) and the non-ligation group (20 patients). All patients had no heart disease, hepatopathy, nephronia, pneumonopathy, hypoproteinemia and no history of radiotherapy. All the patients were followed-up with sonographic evaluation and physical examination for lymphocysts and other postoperative complications at 1, 4, 12, and 24 weeks after operation.

Results: No significant differences were observed between the two groups in pathlogic type, age, height, weight, body surface area, body mass index (BMI), operation duration, estimated blood loss, time to the passage of flatus, total drainage volume, duration of drainage, and duration of hospital stay (P>0.05). The occurrence rate of lymphocysts was significantly lower in the ligation group than in the non-ligation group at one week after operation (26.3% vs. 60.0%, P<0.05). The rates were slightly lower in the ligation group than in the non-ligation group without significant differences after then (31.6% vs. 55.0% at the 4th week), (16.7% vs. 45.0% at the 12th week), (20.0% vs. 27.8% at the 24th week). No significant differences were observed in the occurrence of other postoperative complications between the two groups (P<0.05).

Conclusion: Ligations of the deep inguinal lymph vessels, obturator lymph vessels, common iliac lymph vessels, and the lymph vessels at the crossing of the external iliac and the inter iliac vein can decrease the occurrence of postoperative lymphocysts in short-term period, and will not increase the occurrence of postoperative complications.
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http://dx.doi.org/10.5732/cjc.009.10235DOI Listing
November 2009

[Immunoreactivity of the recombinant protein of Echinococcus granulosus antigen B].

Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi 2009 Apr;27(2):107-10

Medical Research Center, First Teaching Hospital of Xinjiang Medical University, Urumqi 830054, China.

Objective: To express the recombinant antigen B (rAgB) of Echinococcus granulosus (Eg) and investigate its immunoreactivity.

Methods: The rAgB gene fragments were inserted into pET41a (+) prokaryotic vector. The recombinant plasmid was transformed into E. coli BL21 (DE3) and followed by expression of the protein induced by isopropyl beta-D-1-thiogalactopyranoside (IPTG). The protein was purified with sepharose 4B by affinity chromatography, and tested by SDS-PAGE electrophoresis. Its immunoreactivity was examined by Western blotting, and a rapid diagnosis kit for human echinococcosis was used as control.

Results: The constructed recombinant plasmid pET41a-rAgB was identified by PCR, digestion with restriction enzyme and sequencing. The recombinant rAgB-GST was about Mr 40 800 with a purity of 78.4%. Western blotting showed that the positive rate of rAgB-GST reacting with sera of cystic echinococcosis (CE), alveolar echinococcosis (AE), paragonimiasis westermani and clonorchiasis sinensis patients, and healthy persons is 79.2%(95/120), 51.1% (23/45), 0 (0/32), 0 (0/20), and 0 (0/24), respectively. Its overall sensitivity and specificity were 79.2% (95/120) and 81.0% (98/121), respectively, slightly higher than the sensitivity (72.8%, 75/103) and specificity (76.9%, 30/39) of the rapid diagnosis kit for human echinococcosis.

Conclusion: The rAgB-GST recombinant protein is recognized by the sera of CE and AE patients, showing a proper immunoreactivity.
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April 2009

Inhibitory effects of a dihydropyridine calcium channel blocker on renal injury in aldosterone-infused rats.

J Hypertens 2009 Sep;27(9):1855-62

Department of Cardiorenal and Cerebrovascular Medicine, Kagawa University, Japan.

Objectives: Recent in-vitro studies demonstrated that dihydropyridine calcium channel blockers have direct mineralocorticoid receptor antagonistic activity. The present study was conducted to examine the effects of a dihydropyridine calcium channel blocker, azelnidipine, on aldosterone-induced oxidative stress and renal injury.

Methods And Results: Uninephrectomized rats subjected to 6 weeks treatment with aldosterone (0.75 microg/h, subcutaneous) and 1% NaCl (in drinking water) showed higher systolic blood pressure (SBP), urinary excretion of protein (UproteinV), glomerular cell proliferation and renal interstitial fibrosis than vehicle (2% ethanol)-infused rats. Aldosterone-induced renal injury was associated with increased renal cortical content of thiobarbituric acid-reactive substances (TBARS), NAD(P)H oxidase complex formation and mRNA expression of NAD(P)H oxidase membrane components (p22 and gp91). Administration of azelnidipine [3 mg/kg per day, orally (p.o.)] markedly attenuated the aldosterone-induced increases in SBP, UproteinV, renal cortical tissues TBARS content, NAD(P)H oxidase complex formation, mRNA levels of p22 and gp91, and morphological changes. In aldosterone-infused rats, treatment with a nonspecific vasodilator, hydralazine (5 mg/kg per day in drinking water) resulted in a reduction in SBP similar to azelnidipine; however, it did not affect any renal parameters. Treatment with azelnidipine suppressed aldosterone/mineralocorticoid receptor-dependent but not mineralocorticoid receptor-independent superoxide production in cultured rat mesangial cells.

Conclusion: These data suggest that dihydropyridine calcium channel blockers may elicit marked amelioration of aldosterone-induced renal injury through their inhibitory effects on NAD(P)H oxidase-dependent oxidative stress.
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http://dx.doi.org/10.1097/HJH.0b013e32832dda6fDOI Listing
September 2009