Publications by authors named "Danqing Huang"

16 Publications

  • Page 1 of 1

Integrative Analysis of DNA Methylation and Transcriptome Identifies a Predictive Epigenetic Signature Associated With Immune Infiltration in Gliomas.

Front Cell Dev Biol 2021 31;9:670854. Epub 2021 May 31.

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Guangzhou, China.

Glioma is the most common primary brain tumor with poor prognosis and high mortality. The purpose of this study was to use the epigenetic signature to predict prognosis and evaluate the degree of immune infiltration in gliomas. We integrated gene expression profiles and DNA methylation data of lower-grade glioma and glioblastoma to explore epigenetic differences and associated differences in biological function. Cox regression and lasso analysis were used to develop an epigenetic signature based on eight DNA methylation sites to predict prognosis of glioma patients. Kaplan-Meier analysis showed that the overall survival time of high- and low-risk groups was significantly separated, and ROC analysis verified that the model had great predictive ability. In addition, we constructed a nomogram based on age, sex, 1p/19q status, glioma type, and risk score. The epigenetic signature was obviously associated with tumor purity, immune checkpoints, and tumor-immune infiltrating cells (CD8+ T cells, gamma delta T cells, M0 macrophages, M1 macrophages, M2 macrophages, activated NK cells, monocytes, and activated mast cells) and thus, it may find application as a guide for the evaluation of immune infiltration or in treatment decisions in immunotherapy.
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http://dx.doi.org/10.3389/fcell.2021.670854DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8203203PMC
May 2021

Childhood trauma is linked to decreased temporal stability of functional brain networks in young adults.

J Affect Disord 2021 Jul 2;290:23-30. Epub 2021 May 2.

Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Mental Health Institute of Central South University, Changsha, Hunan, China; China National Clinical Research Center on Mental Disorders, Changsha, Hunan, China. Electronic address:

Background: Both childhood trauma and disruptions in brain functional networks are implicated in the development of psychiatric disorders in early adulthood. However, the relationships between these two factors remain unclear. This study aimed to investigate whether and how childhood trauma would relate to changes of functional network dynamics in young adults.

Methods: Resting-state functional magnetic resonance imaging data were collected from 53 young healthy adults, whose childhood trauma histories were assessed by the Childhood Trauma Questionnaire (CTQ). Network switching rate, a measure of stability of dynamic brain networks over time, was calculated at both global and local levels for each participant. Switching rates at both levels were compared between participants with and without childhood trauma, and further correlated with CTQ total score.

Results: In the current sample, 19 (35.8%) participants reported a history of childhood trauma. At the global level, participants with childhood trauma showed significantly higher network switching rates than those without trauma (F = 10.021, p = 0.003). A significant positive correlation was found between network switching rates and CTQ scores in the entire sample (r = 0.378, p = 0.007). At the local level, these effects were mainly observed in the default-mode, fronto-parietal, cingulo-opercular, and occipital subnetworks.

Conclusions: Our study provides preliminary evidence for a possible long-term effect of childhood trauma on brain functional dynamism. These findings may have potential contributions to psychiatric disorders during adulthood.
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http://dx.doi.org/10.1016/j.jad.2021.04.061DOI Listing
July 2021

lncRNA LINC01057 promotes mesenchymal differentiation by activating NF-κB signaling in glioblastoma.

Cancer Lett 2021 02 31;498:152-164. Epub 2020 Oct 31.

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, Guangzhou, 510095, Guangdong, China. Electronic address:

Long non-coding RNAs (lncRNAs) have been potentially identified as new diagnostic markers, prognostic factors and therapeutic targets in cancer. The acquisition of a mesenchymal (MES) phenotype in glioblastomas (GBMs) results into therapeutic resistance and poor clinical outcomes. The correlation between lncRNAs and MES differentiation remains elusive. Here, we report that LINC01057 as a lncRNA is overexpressed in GBMs, especially in MES subtype. LINC01057 knockdown suppresses proliferation, invasion and radioresistance of GBM cells in vitro, and tumor growth in vivo. LINC01057 knockdown leads to loss of MES signature in MES subpopulation of GBM cells, but LINC01057 overexpression promotes MES differentiation in proneural (PN) subpopulation. LINC01057 interacts with IKKα and maintains IKKα nucleus localization, leading to effective chromatin accessibility at NF-κB responsive promoters via histone modification and final NF-κB activation. IKKα knockdown disrupts the effect of LINC01057 overexpression on PN to MES transition (PMT). LINC01057 level is negatively correlated with patient prognosis in MES-subtype GBM. Collectively, our findings uncover LINC01057 as a regulator of NF-κB signaling to promote MES differentiation and a potential target for therapeutic intervention for MES-subtype GBM.
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http://dx.doi.org/10.1016/j.canlet.2020.10.047DOI Listing
February 2021

The effects of mandibular osteotomy on maxillary orthodontic tooth movement and bone remodelling in a rat model.

Eur J Orthod 2020 Sep 15. Epub 2020 Sep 15.

Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Tongji University, Shanghai.

Objectives: The accelerated tooth movement phenomenon after orthognathic surgery has been observed. However, the underlying mechanism remains unclear. There is no experimental study showing the effect of orthognathic surgery on orthodontic tooth movement of the opposing jaw. Therefore, the present study aimed at investigating if mandibular osteotomy enhances maxillary tooth movement and bone remodelling.

Materials And Methods: Fifty-four male Sprague-Dawley rats were randomly divided into two groups: maxillary tooth movement (TM) and maxillary tooth movement + mandibular surgery (TM + MS). The orthodontic force was delivered to move the left maxillary first molar mesially. The surgical intervention was performed on the left mandible. Microcomputed tomography, histological analysis, enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction were used to assess changes at 3, 7, and 21 days after surgery.

Results: The mandibular osteotomy accelerates the rate of maxillary tooth movement with decreased bone volume fraction on the seventh day. Bone resorption was observed on the third and seventh day after mandibular osteotomy. It was found that serum interleukin-1β level increased significantly in the TM + MS group compared with the TM group, as well as the high expression level of cathepsin K and tumour necrosis factor receptor-associated factor 5 of the orthodontic tooth on the third and seventh day after mandibular osteotomy.

Conclusion: Data from the present study suggested that mandibular osteotomy accelerates maxillary osteoclast activity and post-operative tooth movement, providing evidence for accelerated tooth movement phenomenon after orthognathic surgery.
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http://dx.doi.org/10.1093/ejo/cjaa053DOI Listing
September 2020

Left Ventricular Pressure-Strain Loop-Based Quantitative Examination of the Global and Regional Myocardial Work of Patients with Dilated Cardiomyopathy.

Ultrasound Med Biol 2020 10 10;46(10):2834-2845. Epub 2020 Jul 10.

Department of Ultrasonography, People's Hospital of Zhengzhou University, Henan Provincial People's Hospital, Fuwai Central China Cardiovascular Hospital, Zhengzhou, China. Electronic address:

The aim of our prospective pilot study was to explore the distribution characteristics of myocardial work (MW) of patients with dilated cardiomyopathy (DCM) and their clinical value in evaluation of therapeutic effects. Thirty patients with DCM were enrolled in the case group, and 30 healthy patients were randomly allocated to the control group. Global myocardial work (GMW) and regional myocardial work (RMW) of the control and case groups before and after therapy were evaluated by using left ventricular pressure-strain loops and then compared. We found significant differences in GMW and RMW between the control and case groups (p < 0.05). Compared with before therapy, the global work index and 6-min walking distance increased, but LV ejection fraction and global longitudinal strain did not significantly change after therapy. GMW was significantly correlated with LV ejection fraction and global longitudinal strain (p < 0.01). Bland-Altman plot analysis revealed that GMW values were consistent between and within the groups. The results suggest that LV MW values were diffusely impaired in patients with DCM and that the global work index may be used as an indicator in evaluation of therapeutic effects.
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http://dx.doi.org/10.1016/j.ultrasmedbio.2020.06.008DOI Listing
October 2020

A prognostic 11-DNA methylation signature for lung squamous cell carcinoma.

J Thorac Dis 2020 May;12(5):2569-2582

Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China.

Background: Lung squamous cell carcinoma (LUSC), as the second frequent subtype of lung cancer, causes lots of mortalities primarily due to a lack of precise prognostic markers and timely treatment intervention. Previous studies have constructed several risk prognostic models based on DNA methylation sites in multiple tumors, whereas, DNA methylation signature of LUSC remains to be built, and its predictive value need to be evaluated.

Methods: The genome-wide DNA methylation data of LUSC samples was obtained from The Cancer Genome Atlas dataset. Univariate Cox analysis and the least absolute shrinkage and selection operator (LASSO) were implemented to identify DNA methylation sites related to overall survival of LUSC patients. Thus, we performed multivariate Cox regression to establish a DNA methylation signature. The Kaplan-Meier (K-M) survival curves and time-dependent receiver operating characteristic (ROC) curves were plotted to estimate the prognostic power of the signature. Comparison with other known prognostic biomarkers, our DNA methylation signature showed higher predictive specificity and sensitivity. In addition, multivariate Cox regression screened out independent prognostic factors and constructed a nomogram.

Results: Several statistical methods were performed to construct an 11-DNA methylation signature. LUSC patients were divided into low- and high-risk group based on risk score, and high-risk group had a shorter survival time. According to the results of K-M and ROC analyses, the 11-DNA methylation signature showed significant sensitivity and specificity in predicting the LUSC patients' overall survival. Finally, we integrated some independent prognostic factors (risk score, metastasis stage, and tobacco smoking history) to construct a nomogram, which has excellent prognostic power and may provide guidance for the therapeutic strategies.

Conclusions: We constructed the first risk prognosis model based on DNA methylation site in LUSC, which showed better predictive ability. In addition, a nomogram integrating the DNA methylation signature, metastasis stage, and tobacco smoking history was developed.
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http://dx.doi.org/10.21037/jtd.2020.03.31DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7330303PMC
May 2020

LncRNA SNORD3A specifically sensitizes breast cancer cells to 5-FU by sponging miR-185-5p to enhance UMPS expression.

Cell Death Dis 2020 05 7;11(5):329. Epub 2020 May 7.

Affiliated Cancer Hospital & Institute of Guangzhou Medical University; Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation; The State Key Laboratory of Respiratory; Guangzhou Key Laboratory of "Translational Medicine on Malignant Tumor Treatment", Hengzhigang Road 78#, 510095, Guangzhou, Guangdong, China.

Breast cancer is the most common cancer type in women. Long non-coding RNAs (lncRNAs) have been reported as potential new diagnostic markers, prognostic factors, and therapeutic targets in cancer. However, the specific roles and mechanisms of lncRNAs in breast cancer remain to be elucidated. Here we demonstrated the downregulation of lncRNA SNORD3A in breast cancer cells and tissues and verified its non-protein-coding property. SNORD3A overexpression had no effect on cell proliferation but specifically sensitized breast cancer cells to 5-fluorouracil (5-FU) in vitro and in vivo. Mechanistically, SNORD3A exerts its effect via enhancing uridine monophosphate synthetase (UMPS) protein expression. SNORD3A acts as a competing endogenous RNA for miR-185-5p, leading to UMPS protein upregulation. miR-185-5p overexpression disrupted the effect of SNORD3A on chemosensitization to 5-FU in vitro and in vivo. Moreover, Meis1 overexpression transcriptionally promotes SNORD3A expression, and Meis1 is downregulated in breast cancer cells and tissues. In breast cancer tissues, SNORD3A level positively correlates with Meis1 and UMPS protein levels, whereas miR-185-5p level negatively correlates with UMPS protein level. High SNORD3A transcript and Meis1 and UMPS protein levels predicts a better outcome, but high miR-185-5p level predicts a worse outcome in breast cancer patients receiving 5-FU-based chemotherapy. Our findings indicate that Meis1-regulated SNORD3A specifically sensitizes breast cancer cells to 5-FU via enhancing UMPS expression. The SNORD3A-UMPS axis may serve as a potential biomarker and therapeutic target to improve the efficacy of 5-FU-based chemotherapy for breast cancer patients.
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http://dx.doi.org/10.1038/s41419-020-2557-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205983PMC
May 2020

Activity and morphologic changes in the mandible after mandibular osteotomy.

Am J Orthod Dentofacial Orthop 2019 Jan;155(1):40-47

Department of Oral and Maxillofacial Surgery, School & Hospital of Stomatology, Tongji University, Shanghai, China; Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China. Electronic address:

Introduction: Orthognathic surgery accelerates orthodontic tooth movement, and tooth movement accelerates with demineralized bone and accelerated bone remodeling. The purpose of this study was to ascertain whether orthognathic surgery induces accelerated bone remodeling. The research design included a human model and an animal model.

Methods: The levels of serum tartrate resistant acid phosphatase-5b (TRAP) and bone alkaline phosphatase (BALP) were measured in 15 patients after sagittal split ramus osteotomy. For the animal study, 18 rabbits were divided into 6 groups: a control group and 5 surgery groups. The rabbits in the surgery groups had osteotomies in the molar regions of the mandible. Changes in bone mass of the anterior mandibles were examined by microcomputed tomography, and changes in osteoblast and osteoclast numbers were analyzed by real-time polymerase chain reaction, hematoxylin and eosin staining, TRAP staining, and alkaline phosphatase staining.

Results: In the 15 patients, TRAP-5b increased from 1 to 8 weeks postoperatively, and BALP increased significantly in 2 weeks postoperatively. In the rabbits, the levels of mRNA expression of TRAP were increased at 3 weeks, and matrix metalloproteinase 9 was increased at 4 and 8 weeks, whereas mRNA expression of BALP and bone morphogenetic protein 2 were increased at 4 weeks. Bone loss was detected from 1 week postoperatively and reached the maximum at 3 weeks; and bone mass and mechanical structure did not recoverer to preoperative levels until 8 weeks postoperatively.

Conclusions: These findings show active bone remodeling induced by osteotomy.
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http://dx.doi.org/10.1016/j.ajodo.2018.02.016DOI Listing
January 2019

Mandibular osteotomy-induced hypoxia enhances osteoclast activation and acid secretion by increasing glycolysis.

J Cell Physiol 2019 07 12;234(7):11165-11175. Epub 2018 Dec 12.

Department of Oral and Maxillofacial Surgery, School & Hospital of Stomatology, Tongji University, Shanghai, China.

The rapid bone remodeling after osteotomy has been reported for a long time. However, the underlying mechanism promoting the active bone reconstruction was still to be elucidated. Since not only the bone, blood vessels, and supportive tissues, but also the local microenvironment were destroyed, if the changes on the cell metabolism was contributed to the accelerated bone remodeling came into sight. In present study, we found that the mandibular osteotomy in rabbit activated osteoclasts, as well as the expression of hypoxia-inducible factor 1α (HIF-1α) in alveolar bone. Hypoxia or HIF-1α could enhanced osteoclastogenesis, bone absorption, and lactic acid concentration in receptor activator of nuclear factor κΒ ligand-induced RAW264.7 cells. Coincided with the upregulated HIF-1α expression, HIF-driven glycolytic enzymes, such as lactate dehydrogenase A (LDHA), glucokinase (GCK), pyruvate kinase M2 (PKM2), and phosphofructokinase1 (PFK1), were found massively increased in both hypoxic RAW264.7 cells and the alveolar HIF-1α-positive osteoclasts after mandibular osteotomy. Knockdown of HIF-1α suppressed not only the hypoxia-mediated glycolysis, but also the hypoxia-induced acid secretion and bone resorption in RAW264.7 cells. Application of inhibitor on glycolysis gave rise to the similar results as HIF-1α knockdown. Our findings suggested that hypoxia-driven glycolysis in osteoclasts was an adaptive mechanism to permit alveolar bone remodeling after mandibular osteotomy.
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http://dx.doi.org/10.1002/jcp.27765DOI Listing
July 2019

IL-6 Enhances Osteocyte-Mediated Osteoclastogenesis by Promoting JAK2 and RANKL Activity In Vitro.

Cell Physiol Biochem 2017 9;41(4):1360-1369. Epub 2017 Mar 9.

Background/aims: Evidence suggests that IL-6 affects bone mass by modulating osteocyte communication towards osteoclasts. However, the mechanism by which IL-6 enhances osteocyte-mediated osteoclastogenesis is unclear. We aimed to investigate the inflammatory factors in serum after orthodontic surgery and their relationship between osteocytes and osteoclasts.

Methods: Serum was obtained from 10 orthognathic surgery patients, and inflammatory factors were detected by ELISA. We treated the osteocyte-like cell line MLO-Y4 with recombinant mouse IL-6 and IL-6 receptor (IL-6R), and used quantitative RT-PCR and Western blotting to explore Receptor activator of nuclear factor-κB ligand (RANKL) expression at both the mRNA and protein level. MLO-Y4 cells were co-cultured with osteoclast precursor cells, and the formation of osteoclasts was detected by tartrate-resistant acid phosphatase (TRAP) staining. To explore the role of JAK2 in the osteocyte-mediated osteoclastogenesis, AG490, a JAK2 inhibitor, was used to inhibit the JAK2-STAT3 pathway in osteocytes.

Results: In our study, we found that IL-6 and RANKL were stimulated in serum 3-7 days after orthognathic surgery. Therefore, IL-6 and IL-6 receptor enhanced the expression of RANKL at both the mRNA and protein level in MLO-Y4. Furthermore, when MLO-Y4 cells were co-cultured with osteoclast precursor cells, it significantly stimulated osteoclastogenesis. Our study indicated that osteocytes could promote osteoclastic differentiation and the formation of TRAP-positive multinucleated cells after stimulation with IL-6 and IL-6R. Our results also indicated that treatment with IL-6 and IL-6R increased RANKL mRNA expression and the RANKL/OPG expression ratio. Meanwhile, the phosphorylation of Janus kinase 2 (JAK2) and Signal transducer and activator of transcription (STAT3) also correlated with RANKL levels. Furthermore, we investigated the effects of a specific JAK2 inhibitor, AG490, on the expression of RANKL in osteocyte-like MLO-Y4 cells and osteocyte-mediated osteoclastogenesis. The results showed that AG490 inhibited (p)-JAK2 and RANKL expression. Osteoclastic differentiation was decreased after pretreatment in MLO-Y4 with mouse IL-6/IL-6R and AG490; therefore, we concluded that IL-6 increased osteocyte-mediated osteoclastic differentiation by activating JAK2 and RANKL.

Conclusion: The effects of IL-6/il-6R and AG490 on osteocyte-mediated osteoclastogenesis contribute to our understanding of the role of inflammatory factors in the interaction between osteocytes and osteoclast precursors. IL-6 and RANKL are key factors for bone remodelling after the orthodontic surgery, and their roles in bone remodelling may be fundamental mechanisms accelerating tooth movement by orthodontic surgery.
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http://dx.doi.org/10.1159/000465455DOI Listing
June 2017

Expression of NF-κB-inducing kinase in breast carcinoma tissue and its clinical significance.

Int J Clin Exp Pathol 2015 1;8(11):14824-9. Epub 2015 Nov 1.

Department of Oncology, The Affiliated Hospital of Hubei Institute of Science and Technology, Huangshi Central Hospital Huangshi, Hubei, China.

Objective: To investigate the expression of nuclear factor-κB-inducing kinase (NIK) in breast carcinoma tissue and tumor-adjacent normal breast tissue and evaluate its clinical significance.

Methods: Surgically resected tissue specimens were collected from 82 patients with breast carcinoma who underwent surgical treatment at our hospital from March 2001 to December 2009. The diagnoses of all patients were confirmed by postoperative pathological examinations. NIK protein expression in breast carcinoma tissue and adjacent normal breast tissue was detected by immunohistochemistry; the association between NIK expression and the clinicopathological features and prognosis of patients with breast carcinoma was examined.

Results: The positive expression rate of NIK in breast carcinoma tissue was significantly higher than that in normal tissue (63.4% vs. 25.6%, P < 0.05). Additionally, NIK expression showed no relationship to the tumor size, age, degree of differentiation, or pathological type; however, it showed a significant correlation with lymph node metastasis and the clinical stage of patients (P < 0.05). The five-year survival rate was significantly lower in breast carcinoma patients who were positive for NIK expression than in those who were negative for NIK expression (P = 0.006).

Conclusion: NIK expression was significantly increased in the tumor tissue of patients with breast carcinoma, which may be an important factor that affects the prognosis of these patients.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713597PMC
October 2016

Poly (N-Isopropylacrylamide) microgel-based optical devices for humidity sensing.

Anal Chim Acta 2015 Oct 8;898:101-8. Epub 2015 Oct 8.

Department of Chemistry, University of Alberta, Edmonton, AB, T6G 2G2, Canada. Electronic address:

Optical sensors for environmental humidity have been constructed from poly (N-isopropylacrylamide)-co-acrylic acid (pNIPAm-co-AAc) microgels. The devices were constructed by first depositing a monolithic layer of pNIPAm-co-AAc microgels on a Au-coated glass substrate followed by the addition of another Au layer on top. The resultant assembly showed visual color, and exhibited multipeak reflectance spectra. We found that the thickness of the device's microgel layer depended on environmental humidity, which corresponded to a change in the device's optical properties. Specifically, at low humidity the microgel layer was collapsed, while it absorbed water from the atmosphere (and swelled) as the humidity increased. Additionally, we investigated how the deposition of the hygroscopic polymer poly (diallyldimethylammonium chloride) (pDADMAC) onto the microgel layer (prior to final Au layer deposition) influenced the devices humidity response. We found that the devices were more sensitive to humidity as the number of pDADMAC layers in the device increased. Finally, we evaluated the device performance at various temperatures, and found that the sensitivity was enhanced at low temperature, although the response was more linear at elevated temperature.
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http://dx.doi.org/10.1016/j.aca.2015.09.039DOI Listing
October 2015

[Analysis of CSF1R gene mutation in a Chinese family with hereditary diffuse leukoencephalopathy with neuroaxonal spheroids].

Zhonghua Yi Xue Yi Chuan Xue Za Zhi 2015 Apr;32(2):208-12

Department of Rehabilitation, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.

Objective: To identify potential mutation of the colony stimulating factor 1 receptor gene (CSF1R) in a large Chinese family affected with hereditary diffuse leukoencephalopathy with spheroids (HDLS) and analyze the genotype-phenotype correlation.

Methods: The proband was evaluated physically and radiologically to ascertain the HDLS phenotype. Genomic DNA was extracted from peripheral blood samples from family members. The coding region of the CSF1R gene was amplified with PCR and subjected to direct DNA sequencing.

Results: There were 9 affected members (5 alive) in this five-generation family (1 member had died during the follow-up). A missense mutation c.2563C>A (p.P855T) of the CSF1R gene has been identified in the proband. The same mutation was identified in 3 affected and 1 unaffected members of the family.

Conclusion: The family was consistent with autosomal dominant inheritance. CSF1R gene mutation is also a disease-causing mutation in Chinese patients.
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http://dx.doi.org/10.3760/cma.j.issn.1003-9406.2015.02.012DOI Listing
April 2015

Effect of HIF-1α on biological activation of human tongue squamous cell carcinoma SCC-15 cells in vitro.

Int J Oncol 2015 26;46(6):2346-54. Epub 2015 Mar 26.

Laboratory of Oral Biomedical Science and Translational Medicine, School of Stomatology, Tongji University, Middle Yanchang Road 399, Shanghai 200072, P.R. China.

Hypoxia-inducible factor-1α (HIF-1α) is a key regulator for tumor cells and tissues to adapt to hypoxic condition. Suppressing the expression of HIF-1α is important to evaluate its effect on cancer cells. This study was carried out to analyze the effect of HIF-1α on the biological activation of human tongue squamous cell carcinoma (TSCC) SCC-15 cells. In this experiment, deferoxamine mesylate (DFO) was used to induce hypoxic condition. HIF-1α gene was suppressed by lentiviral vector. The effect of the level of HIF-1α expression was tested on the proliferation, cell cycle, cell apoptosis and cell invasion of SCC-15 cells. We demonstrated that SCC-15 cells showed a more aggressive phenotype after treated with DFO. Additionally, DFO was able to induce the expression of HIF-1α protein. Lentiviral vector can effectively inhibit HIF-1α expression on mRNA and protein level. Under normoxic or hypoxic conditions, downregulation of HIF-1α for SCC-15 cells induced cell apoptosis and inhibited growth and invasion. These results showed that suppressing the expression of HIF-1α inhibited the aggressive potential of SCC-15 cells under normoxic and hypoxic condition. Thus, finding an effective and safe pathway to inhibit the expression of HIF-1α can help us to improve the survival rate of human TSCC patients.
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http://dx.doi.org/10.3892/ijo.2015.2934DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441294PMC
February 2016

Cocaine- and amphetamine-regulated transcript promotes the differentiation of mouse bone marrow-derived mesenchymal stem cells into neural cells.

BMC Neurosci 2011 Jul 14;12:67. Epub 2011 Jul 14.

Department of Neurology, Drum Tower Hospital of Nanjing Medical University, 321 Zhongshan Road, Nanjing, Jiangsu 210008, P.R. China.

Background: Neural tissue has limited potential to self-renew after neurological damage. Cell therapy using BM-MSCs (bone marrow mesenchymal stromal cells) seems like a promising approach for the treatment of neurological diseases. However, the neural differentiation of stem cells influenced by massive factors and interactions is not well studied at present.

Results: In this work, we isolated and identified MSCs from mouse bone marrow. Co-cultured with CART (0.4 nM) for six days, BM-MSCs were differentiated into neuron-like cells by the observation of optical microscopy. Immunofluorescence demonstrated that the differentiated BM-MSCs expressed neural specific markers including MAP-2, Nestin, NeuN and GFAP. In addition, NeuN positive cells could co-localize with TH or ChAT by double-labled immunofluorescence and Nissl bodies were found in several differentiated cells by Nissl stain. Furthermore, BDNF and NGF were increased by CART using RT-PCR.

Conclusion: This study demonstrated that CART could promote the differentiation of BM-MSCs into neural cells through increasing neurofactors, including BNDF and NGF. Combined application of CART and BM-MSCs may be a promising cell-based therapy for neurological diseases.
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http://dx.doi.org/10.1186/1471-2202-12-67DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199873PMC
July 2011

Antitumor activity of the aqueous extract from Sedum sarmentosum Bunge in vitro.

Cancer Biother Radiopharm 2010 Feb;25(1):81-8

Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.

Objective: Sedum sarmentosum Bunge, a Chinese herb, is mainly used for the treatment of chronic viral hepatitis in China, The aim of this work was to examine the cytotoxic activity of S. sarmentosum (aqueous extract, AE) against a human hepatoma cell line (HepG2) in culture.

Materials And Methods: Cell-proliferation ability was determined by the MTT method. Cell-cycle changes and earlier period apoptotic rate of HepG2 cells were detected by flow cytometry. Apoptosis of cultured HepG2 cells induced by AE were observed with a classic laddering pattern on agarose gel electrophoresis. The mRNA levels of Bcl-2 and vascular endothelial growth factor (VEGF) were determined by reverse-transcriptase polymerase chain reaction. The protein expressions of Bcl-2, VEGF, and p-STAT3 were valued by immunocytochemistry.

Results: The application of AE to the HepG2 cell culture caused a significant, dose-dependent inhibition of cancer cell growth. It was found that the AE treatment induced apoptosis of the cancer cells, although no changes were found after AE treatment for 48 hours in the HepG2 cell cycle. The mRNA and protein expressions of Bcl-2 and VEGF and the protein level of p-STAT3 were significantly decreased after the AE treatment for 48 hours.

Conclusions: This study suggests that AE of S. sarmentosum has potential in preventing and inhibiting effects on hepatocellular carcinoma, which is associated with apoptosis of the cancer cells.
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http://dx.doi.org/10.1089/cbr.2009.0632DOI Listing
February 2010