Publications by authors named "Qingbing Meng"

10 Publications

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[Early reperfusion strategy selection and prognosis analysis in patients with acute ST segment elevation myocardial infarction: based on the data of 49 hospitals in Hebei Province].

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2021 May;33(5):578-581

Department of Emergency, Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China. Corresponding author: Gao Hengbo, Email:

Objective: To explore the selection of strategies for early reperfusion therapy and its impact on prognosis in patients with acute ST segment elevation myocardial infarction (STEMI).

Methods: The treatment data and 3-year follow-up results of acute myocardial infarction (AMI) patients in 49 hospitals in Hebei Province from January to December 2016 were collected. Patients with STEMI who received either intravenous thrombolytic therapy (ITT) or primary percutaneous coronary intervention (PPCI) within 12 hours of onset were enrolled. Baseline data, the time from the first diagnosis to the start of reperfusion (FMC2N for ITT patients and FMC2B for PPCI patients), vascular recanalization rate, in-hospital mortality, 1-year mortality, and 3-year mortality were compared between ITT and PPCI groups. The efficacy and prognosis of ITT and PPCI at different starting time of reperfusion (FMC2N ≤ 30 minutes, FMC2N > 30 minutes, FMC2B ≤ 120 minutes, FMC2B > 120 minutes) were analyzed.

Results: A total of 1 371 STEMI patients treated with ITT or PPCI were selected, including 300 patients in the ITT group and 1 071 patients in the PPCI group. 1 055 patients were actually followed up (205 patients in the ITT group and 850 patients in the PPCI group), with a rate of 79.4%. There were no significant differences in age, gender, and previous history between the two groups. The time from the first diagnosis to the start of reperfusion in the ITT group was shorter than that in the PPCI group [minutes: 63 (38, 95) vs. 95 (60, 150), U = -9.286, P = 0.000], but was significantly longer than the guideline standard. Compared with the ITT group, the vascular recanalization rate in the PPCI group was higher [95.5% (1 023/1 071) vs. 88.3% (265/300), P < 0.01], and in-hospital mortality was lower [2.1% (22/1 071) vs. 6.7% (20/300), P < 0.01], but there were no significant differences in the 1-year mortality and 3-year mortality [5.3% (45/850) vs. 4.4% (9/205), 9.5% (81/850) vs. 9.3% (19/205), both P > 0.05]. Between ITT group and PPCI group with different reperfusion starting time, the FMC2N > 30 minutes group had the lowest vascular recanalization rate and the highest in-hospital mortality. Pairwise comparison showed that the vascular recanalization rate of the FMC2B ≤ 120 minutes group and the FMC2B > 120 minutes group were significantly higher than those of the FMC2N > 30 minutes group [95.5% (654/685), 95.6% (369/386) vs. 88.0% (220/250), both P < 0.008], the in-hospital mortality was significantly lower than that of the FMC2N > 30 minutes group [2.0% (14/685), 2.1% (8/386) vs. 7.6% (19/250), both P < 0.008]. There was no significant difference in 1-year mortality (χ = 2.507, P = 0.443) and 3-year mortality (χ = 2.204, P = 0.522) among the four groups.

Conclusions: For STEMI patients within 12 hours of onset, reperfusion therapy should be performed as soon as possible. PPCI showed higher infarct related artery opening rate and lower in-hospital mortality compared with ITT, and had no effect on 1-year and 3-year mortality.
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http://dx.doi.org/10.3760/cma.j.cn121430-20210207-00228DOI Listing
May 2021

The effects of ω-3 fish oil emulsion-based parenteral nutrition plus combination treatment for acute paraquat poisoning.

J Int Med Res 2019 Feb 5;47(2):600-614. Epub 2018 Nov 5.

1 Emergency Department, Second Hospital of Hebei Medical University, Xinhua District, Shijiazhuang, Hebei, China.

Objective: To investigate the effects of parenteral nutrition (PN) including ω-3 fish-oil emulsion on nutritional state, inflammatory response, and prognosis in patients with acute paraquat poisoning.

Methods: Patients randomized to receive medium chain triglycerides (MCT)/long chain triglycerides (LCT)-based PN (control group) or MCT/LCT-based PN containing ω-3 fish-oil emulsion (intervention group) were compared for 90-day survival and short-term treatment efficacy.

Results: Tumour necrosis factor-α levels were significantly lower in the intervention group ( n = 101) versus controls ( n = 73) on treatment days 4 and 7. Intervention group C-reactive protein (CRP) levels were significantly increased on day 4, decreased to baseline (day 1) levels on day 7, and were significantly lower than baseline on day 10. Control group CRP levels were significantly increased on days 4 and 7 versus baseline, and returned to baseline levels on day 10. On day 7, retinol binding protein had recovered to baseline levels in the intervention group only. Intervention group mortality rate (36.6%) was significantly lower than controls (57.5%). ω-3 fish-oil PN was associated with reduced risk of death (hazard ratio 0.52; 95% confidence interval 0.33, 0.82).

Conclusion: In patients with acute paraquat poisoning, MCT/LCT with ω-3 fish-oil emulsion PN plus combination treatment advantageously attenuated the inflammatory response, modified the nutritional state, and was associated with significantly improved 90-day survival versus treatment without ω-3 fish oil.
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http://dx.doi.org/10.1177/0300060518806110DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6381463PMC
February 2019

The effects of TRAF6 on proliferation, apoptosis and invasion in osteosarcoma are regulated by miR-124.

Int J Mol Med 2018 May 5;41(5):2968-2976. Epub 2018 Feb 5.

Orthopedics Department, Yancheng City No. 1 People's Hospital, Yancheng, Jiangsu 224005, P.R. China.

The present study aimed to verify tumor necrosis factor receptor‑associated factor 6 (TRAF6) as the target gene of microRNA-124 (miR-124). In addition, the expression of miR‑124 was investigated in osteosarcoma tissues and cells, and its effects on the biological characteristics of osteosarcoma cells were determined, in order to provide an experimental and theoretical basis for the application of TRAF6 in the treatment of osteosarcoma. A fluorescence reporter enzyme system was used to verify TRAF6 as a target gene of miR‑124, and western blotting was used to detect the effects of miR‑124 on the protein expression levels of TRAF6 in cells. The expression levels of miR‑124 were detected in osteosarcoma tissues and an osteosarcoma cell line (MG‑63) by quantitative polymerase chain reaction (qPCR). In addition, a total of 48 h post‑transfection of MG‑63 cells with a miR‑124 mimic, qPCR was used to detect the expression levels of miR‑124, and the effects of miR‑124 on the viability of MG‑63 human osteosarcoma cells was determined using the MTT method. The effects of miR‑124 on the cell cycle progression and apoptosis of MG‑63 cells were analyzed by flow cytometry, whereas the effects of miR‑124 on the migration of MG‑63 cells was detected using the Transwell invasion chamber analysis method. A TRAF6 recombinant expression plasmid (pcDNA3.1‑TRAF6) was also constructed, and MG‑63 cells were transfected with the recombinant plasmid and a miR‑124 mimic, in order to further validate the biological role of miR‑124 via the regulation of TRAF6. The results of the present study indicated that, compared with in the normal control group, the expression levels of miR‑124 were significantly increased in MG‑63 cells transfected with a miR‑124 mimic (P<0.01). In addition, the luciferase reporter gene system demonstrated that, compared with in the control group, relative luciferase activity was significantly reduced in the miR‑124 mimic group (P<0.01). The results of MTT analysis indicated that cell viability was also significantly reduced in response to the overexpression of miR‑124 in MG‑63 cells (P<0.01). Flow cytometric analysis demonstrated that the proportion of cells in S phase and G2/M phase was significantly decreased (P<0.01) in cells overexpressing miR‑124, and the number of apoptotic cells was significantly increased (P<0.01). Furthermore, the results of the Transwell invasion assay suggested that the number of invasive cells was significantly decreased following enhanced expression of miR‑124 (P<0.01). In MG‑63 cells overexpressing miR‑124 and TRAF6, the results of MTT, flow cytometric and Transwell assay analyses demonstrated that the overexpression of TRAF6 had the opposite biological effects compared to miR‑124 overexpression. In conclusion, the present study indicated that the expression levels of miR‑124 were downregulated in human osteosarcoma tissues and cells, and that miR‑124 is associated with negative regulation of TRAF6 expression; therefore, the role of TRAF6 in primary osteosarcoma may be regulated by miR‑124. Therapeutic strategies that enhance miR‑124 expression or inhibit TRAF6 expression may be beneficial for the treatment of patients with osteosarcoma.
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http://dx.doi.org/10.3892/ijmm.2018.3458DOI Listing
May 2018

MicroRNA-19 contributes to the malignant phenotypes of osteosarcoma in vitro by targeting Pax6.

Tumour Biol 2018 Jan;40(1):1010428317744704

1 Orthopedics Department, Yancheng City No. 1 People's Hospital, Yancheng, P.R. China.

This study was conducted to detect the expression of miR-19 and Pax6 (Paired box protein 6) in human osteosarcoma cells and the effects on biological characteristics of osteosarcoma cells. Quantitative real-time polymerase chain reaction was used to detect the expression of Pax6 and miR-19 in normal human osteoblasts (hFOB 1.19) and osteosarcoma cell lines (U2OS, Saos-2, and MG-63). Results showed that miR-19 was significantly upregulated in osteosarcoma cell lines compared with that in hFOB 1.19 cells, while the expression of Pax6 messenger RNA was significantly downregulated. Pax6 was defined as the target gene of miR-19 which was validated by luciferase reporter gene analysis. Results indicated that miR-19 had an interaction with Pax6 3'-untranslated region. At the same time, the protein expression of Pax6 was significantly decreased in the MG-63 cells transfected with miR-19 mimic and was notably enhanced in osteosarcoma MG-63 cells transfected with miR-19 inhibitor. These data suggested that Pax6 was a target of miR-19 in osteosarcoma MG-63 cells. The effects of miR-19 on the biological behavior of MG-63 cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and Transwell assay. Results showed that the downregulation of miR-19 inhibited cell viability, reduced the percentage of cells in S phase and the number of cells passing through the Transwell chamber, and increased the number of apoptotic cells. Western blot analysis showed that the inhibition of miR-19 significantly increased the expression of epithelial proteins (E-cadherin and β-catenin) and decreased the expression of mesenchymal protein (Vimentin), extracellular signal-regulated kinase, and phosphorylated extracellular signal-regulated kinase in MG-63 cells. MiR-19 inhibitor and Pax6 small interfering RNA were simultaneously transfected into MG-63 cells. Results from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and Transwell assay demonstrated that the inhibition of Pax6 expression in MG-63 cells could reverse the cell biological effects induced by the inhibition of miR-19 expression. Based on these findings, it was suggested that miR-19, upregulated in osteosarcoma cells, negatively regulated the expression of Pax6, which can promote the malignant phenotypes of osteosarcoma cells via activation of the extracellular signal-regulated kinase signaling pathways. Therefore, miR-19/Pax6 may offer potential for use as a target for the treatment of osteosarcoma.
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http://dx.doi.org/10.1177/1010428317744704DOI Listing
January 2018

Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema.

Exp Ther Med 2016 Mar 29;11(3):993-997. Epub 2015 Dec 29.

Department of Emergency Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.

The present study aimed to investigate the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and interleukin (IL)-6 in the lung tissue of a rat model of acute pulmonary edema induced by acute hypoxia, and its pathophysiological significance. A total of 48 adult Wistar rats were randomly divided into group A, a normal group; group B, a model of acute pulmonary edema induced by hypoxia for 24 h; group C, a model of acute pulmonary edema induced by hypoxia for 48 h; and group D, a model of acute pulmonary edema induced by hypoxia for 72 h. The rats in groups B-D were intraperitoneally injected with 6% ammonium chloride to establish the model of acute pulmonary edema, and were subsequently sacrificed following successful modeling for 24, 48 and 72 h. The plasma of rats was isolated and the lungs of the rats were removed. Subsequently, a 10% lung homogenate was prepared and the contents and the activities of MDA, SOD and IL-6 in the lung tissue and IL-6 in the plasma were detected by enzyme-linked immunosorbent assay. MDA and IL-6 expression levels increased and SOD activity decreased in the lung tissue in group B as compared with group A; however the difference did not reach significance (P>0.05). MDA, IL-6 and SOD levels in the lung tissue of rats were significantly altered following the increased duration of pulmonary edema in groups C and D, as compared group A (P<0.05). The plasma IL-6 levels of the rats in groups B-D significantly increased, as compared with those in group A (P<0.05). In conclusion, the results of the present study demonstrated that the incidence of acute pulmonary edema may be associated with oxidative stress. Furthermore, decreased antioxidant capacity and increased free radical levels may be associated with pulmonary edema, as in the present study the levels of IL-6, SOD and MDA in the lung tissue were observed to be associated with the pathological changes of the disease.
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http://dx.doi.org/10.3892/etm.2015.2962DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4774324PMC
March 2016

Downregulation of HMGA2 inhibits cellular proliferation and invasion, improves cellular apoptosis in prostate cancer.

Tumour Biol 2016 Jan 5;37(1):699-707. Epub 2015 Aug 5.

Orthopedics Department, The Fourth Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, People's Republic of China.

Prostate cancer is the most commonly diagnosed cancer among men and is the second leading cause of cancer-associated deaths among men in the world. Unfortunately, treatment failures are common due to the metastasis and chemoresistance, but the underlying molecular mechanism remains unclear. Accumulating evidence has indicated that the deregulation of DNA-binding protein High Mobility Group A2 (HMGA2) is associated with the development and progression of cancer. This study aimed to explore the expression of HMGA2 in prostate cancer tissues and its correlation to the clinical pathology of prostate cancer, and to discuss the role of HMGA2 in the development of prostate cancer. The results showed that the expression of HMGA2 messenger RNA (mRNA) in the prostate cancer tissues and cells was significantly higher than that in normal prostate tissues and cells (p < 0.05), and the positive expression rate of HMGA2 mRNA in the prostate cancer tissues from patients with positive lymph node metastasis or with high Gleason grade was significantly higher than that from patients with negative lymph node metastasis or with low Gleason grade (p < 0.05). In order to explore the role of HMGA2 in prostate cancer, the expression of HMGA2 in the human prostate cancer PC3 cell line was downregulated by RNA interference. Then, the changes in proliferation, apoptosis, invasion, and migration of PC3 cells were examined by MTT test, PI staining, Annexin V-FITC staining, and Transwell chamber assay. Results showed that the abilities of proliferation, invasion, and migration were suppressed in HMGA2 knockdown PC3 cells, and the abilities of apoptosis were enhanced in HMGA2 knockdown PC3 cells. The expression of cyclin A and vimentin was downregulated in HMGA2 knockdown PC3 cells, and the expression of caspase 3 and E-cadherin was upregulated in HMGA2 knockdown PC3 cells. Taken together, the overexpression of HMGA2 in prostate cancer might be related to the tumorigenesis, invasion, and metastasis of prostate cancer, the downregulation of HMGA2 could inhibit cellular proliferation, invasion, and metastasis, and improve cellular apoptosis in prostate cancer, which might be a potential target for the treatment of prostate cancer.
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http://dx.doi.org/10.1007/s13277-015-3853-9DOI Listing
January 2016

HMGB1 promotes cellular proliferation and invasion, suppresses cellular apoptosis in osteosarcoma.

Tumour Biol 2014 Dec 29;35(12):12265-74. Epub 2014 Aug 29.

Orthopedics Department, Yancheng City No.1 People's Hospital, 16 Yue-He Road, Yancheng, 224005, Jiangsu Province, People's Republic of China.

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. Unfortunately, treatment failures are common due to the metastasis and chemoresistance, but the underlying molecular mechanism remains unclear. Accumulating evidence indicated that the deregulation of DNA-binding protein high-mobility group box 1 (HMGB1) was associated with the development of cancer. This study aimed to explore the expression of HMGB1 in osteosarcoma tissues and its correlation to the clinical pathology of osteosarcoma and to discuss the role of HMGB1 in the development of osteosarcoma. The results from RT-PCR and Western blot showed that the expression rate of HMGB1 messenger RNA (mRNA) and the expression of HMGB1 in the osteosarcoma tissues were significantly higher than those in normal bone tissue (p < 0.05), the expression rate of HMGB1 mRNA and the expression of HMGB1 in the carcinoma tissues with positive lung metastasis were significantly higher than those without lung metastasis (p < 0.05), and with increasing Enneking stage, the expression rate of HMGB1 mRNA and the expression of HMGB1 also increased (p < 0.05). In order to explore the role of HMGB1 in osteosarcoma, the expression of HMGB1 in the human osteosarcoma MG-63 cell line was downregulated by the technique of RNA interference. Western blot results showed that the protein expression of HMGB1 was significantly decreased in the MG-63 cells from HMGB1-siRNA transfection group (p < 0.05), which suggested that HMGB1 was successfully downregulated in the MG-63 cells. Then the changes in proliferation, apoptosis, and invasion of MG-63 cells were examined by MTT test, PI staining, annexin V staining, and transwell chamber assay. Results showed that the abilities of proliferation and invasion were suppressed in HMGB1 knockdown MG-63 cells, and the abilities of apoptosis were enhanced in HMGB1 knockdown MG-63 cells. The expression of cyclin D1, MMP-9 was downregulated in HMGB1 knockdown MG-63 cells, and the expression of caspase-3 was upregulated in HMGB1 knockdown MG-63 cells. Taken together, the overexpression of HMGB1 in osteosarcoma might be related to the tumorigenesis, invasion, and metastasis of osteosarcoma, which might be a potential target for the treatment of osteosarcoma.
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http://dx.doi.org/10.1007/s13277-014-2535-3DOI Listing
December 2014

SASH1 regulates proliferation, apoptosis, and invasion of osteosarcoma cell.

Mol Cell Biochem 2013 Jan 29;373(1-2):201-10. Epub 2012 Oct 29.

Orthopedics Department, Yancheng City No. 1 People's Hospital, 16 Yue-He Road, Yancheng 224005, Jiangsu, People's Republic of China.

SASH1, a member of the SLY-family of signal adapter proteins, is a candidate tumor suppressor in breast and colon cancer. The SASH1 protein possesses both the SH3 and SAM domains, indicating that it may play an important role in intracellular signal transduction. Reduced expression of SASH1 is closely related to tumor growth, invasion, metastasis, and poor prognosis. However, the biological role of SASH1 remains unknown in osteosarcoma. To unravel the function of SASH1, we explored the expression of SASH1 in osteosarcoma tissues and its correlation to the clinical pathology of osteosarcoma and analyzed the relationship between SASH1 expression and cell cycle, apoptosis and invasion of osteosarcoma MG-63 cells, using the flow cytometry analysis and transwell invasion chamber experiments. Furthermore, the effect of SASH1 on the expression of cyclin D1, caspase-3, matrix metalloproteinase (MMP)-9 were observed by western blot. Our results showed that the expression rate of SASH1 mRNA in osteosarcoma tissues was significantly lower than that in normal bone tissue (p = 0.000), that the expression rate of SASH1 mRNA in the carcinoma tissues from patients with lung metastasis was significantly lower than that from patients without lung metastasis (p = 0.041), and that the expression rate of SASH1 mRNA also decreased with increasing Enneking stage (p = 0.032). However, the mRNA expression of SASH1 in osteosarcoma was independent of the patient's gender, age, and tumor size (p = 0.983, 0.343, 0.517, respectively). The SASH1 protein displayed a down-regulation in osteosarcoma tissues compared to normal bone tissue (p = 0.000), displayed a down-regulation in osteosarcoma tissues from patients with lung metastasis compared to from patients without lung metastasis (p = 0.000), and displayed a gradual decrease with increasing Enneking stage (p = 0.000). In addition, the MG-63 cells from pcDNA3.1-SASH1 group exhibited significantly reduced cell viability, proliferation, and invasive ability compared to the empty vector group and blank control group (p = 0.023, 0.001, respectively), and there was no difference between the empty vector group and blank control group. The pcDNA3.1-SASH1 group displayed significantly more apoptotic cells than the empty vector group and blank control group (p = 0.004). The expression of cyclin D1, MMP-9 displayed a down-regulation in MG-63 cells from pcDNA3.1-SASH1 group compared to the empty vector group and blank control group (p = 0.000, 0.001, respectively) and the expression levels of caspase-3 displayed an up-regulation in MG-63 cells from pcDNA3.1-SASH1 group compared to the empty vector group and blank control group (p = 0.000). Taken together, these data indicated that the overexpression of SASH1 might be associated with the inhibition of growth, proliferation, and invasion of MG-63 cells and the promotion of apoptosis of MG-63 cells.
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http://dx.doi.org/10.1007/s11010-012-1491-8DOI Listing
January 2013

TRAF6 regulates proliferation, apoptosis, and invasion of osteosarcoma cell.

Mol Cell Biochem 2012 Dec 12;371(1-2):177-86. Epub 2012 Aug 12.

Orthopedics Department, Yancheng City No. 1 People's Hospital, 16 Yue-He Road, Yancheng, Jiangsu 224005, People's Republic of China.

TRAF6, a unique tumor necrosis factor receptor-associated factor (TRAF) family member, possesses a unique receptor-binding specificity that results in its crucial role as the signaling mediator for TNF receptor superfamily and interleukin-1 receptor/Toll-like receptor superfamily. TRAF6 plays an important role in tumorigenesis, invasion and metastasis. This study aimed to explore the expression of TRAF6 in osteosarcoma tissues and its correlation to the clinical pathology of osteosarcoma and to discuss the relationship between TRAF6 expression and osteosarcoma invasion. These data will provide the experimental base for the biological treatment of osteosarcoma in the future. Using RT-PCR and Western blot, the results showed that the expression rate of TRAF6 mRNA in osteosarcoma tissues was significantly higher than that in normal bone tissue (p < 0.05), that the expression rate of TRAF6 mRNA in the carcinoma tissues from patients with lung metastasis was significantly higher than that from patients without lung metastasis (p < 0.05), and that the expression rate of TRAF6 mRNA also increased with increasing Enneking stage (p < 0.05). However, the mRNA expression of TRAF6 in osteosarcoma was independent of the patient's gender, age, and tumor size (p > 0.05). The TRAF6 protein displayed an up-regulation in osteosarcoma tissues compared to normal bone tissue (p < 0.05), displayed an up-regulation in osteosarcoma tissues from patients with lung metastasis compared to from patients without lung metastasis (p < 0.05), and displayed a gradual increase with increasing Enneking stage (p < 0.05). By the technique of RNA interference, the expression of TRAF6 in the human osteosarcoma MG-63 cell line was down-regulated, and the invasive ability of MG-63 cells was examined. The results showed that TRAF6 protein expression was significantly decreased in the MG-63 cells from TRAF6 siRNA-transfected group (p < 0.05), and the proliferation ability of MG-63 cells and the number of MG-63 cells that passed through the Transwell chamber were significantly lower than that in the non-transfected control group as well as the transfected control group (p < 0.05). In addition, the percentage of MG-63 cells undergoing apoptosis was significantly higher in the TRAF6 siRNA-transfected group compared with the non-transfected control group as well as the transfected control group (p < 0.05). The expression of p-p65, cyclin D1, MMP-9 was down-regulated in the MG-63 cells from TRAF6 siRNA-transfected group. The expression of caspase 3 was up-regulated in the MG-63 cells from TRAF6 siRNA-transfected group compared to the non-transfected control group as well as the transfected control group (p < 0.05). To make a long story short, the overexpression of TRAF6 in osteosarcoma might be related to the tumorigenesis, invasion of osteosarcoma.
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http://dx.doi.org/10.1007/s11010-012-1434-4DOI Listing
December 2012

Regulation of inflammatory response in human chondrocytes by lentiviral mediated RNA interference against S100A10.

Inflamm Res 2012 Nov 14;61(11):1219-27. Epub 2012 Jul 14.

Department of Orthopaedics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China.

Objective: The aim of the present study was to evaluate the effects of S100A10 silencing on the inflammatory response in human chondrocytes (HCs).The inflammation induced by lipopolysaccharide (LPS) was investigated in HCs in which the S100A10 was blocked with a lentiviral shRNA vector.

Methods: A lentiviral shRNA vector targeting S100A10 was constructed and packaged to effectively block S100A10 expression in HCs. HCs were infected with the lentivirus. S100A10 expression levels in HCs were detected by western blot analysis. Enzyme-linked immunosorbent assay (ELISA) was employed to evaluate the change of cytokine secretion levels. The effects of S100A10 silencing on the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathway were also determined by western blot analysis. In addition, fluo-3-AM was used to demonstrate the change in calcium mobilization.

Results: Lentivirus effectively infected the HCs and inhibited the expression of S100A10. HCs with downregulated S100A10 showed significantly decreased production of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-10. S100A10 silencing markedly suppressed the activation of MAPKs induced by LPS. Furthermore, the calcium concentration increase in HCs stimulated by LPS was also inhibited by S100A10 knockdown.

Conclusion: Our investigation demonstrated that S100A10 might be considered as a potential target for anti-inflammatory treatment.
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http://dx.doi.org/10.1007/s00011-012-0519-6DOI Listing
November 2012
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