Pla No 161 Center Hospital

Jianghan District, China

Pla No 161 Center Hospital

Jianghan District, China
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Li Y.,Chinese PLA General Hospital | Li Y.,Kunming General Hospital of Chengdu Military Command | Geng P.,Chinese PLA General Hospital | Jiang W.,Academy of Military Medical science | And 7 more authors.
Tumor Biology | Year: 2014

Radiation resistance is a major problem preventing successful treatment. Therefore, identifying sensitizers is vitally important for radiotherapy success. Epigenetic events such as DNA methylation have been proposed to mediate the sensitivity of tumor therapy. In this study, we investigated the influence of demethylating agent 5-Aza-2′-deoxycytidine (5-Aza-CdR) on the radiosensitivity of human osteosarcoma cell lines. 5-Aza-CdR was capable of sensitizing three osteosarcoma cells to irradiation in a time-dependent manner, with the maximum effect attained by 48 h. Pretreatment with 5-Aza-CdR synchronized cells in G2/M phase of the cell cycle and enhanced irradiation-induced apoptosis compared with irradiation alone in SaOS2, HOS, and U2OS cells. Moreover, 5-Aza-CdR restored mRNA expressions of 14-3-3σ, CHK2, and DAPK-1 in the three cells, accompanied with demethylation of their promoters. These findings demonstrate that demethylation with 5-Aza-CdR increases radiosensitivity in some osteosarcoma cells through arresting cells at G2/M phase and increasing apoptosis, which is partly mediated by upregulation of 14-3-3σ, CHK2, and DAPK-1 genes, suggesting that 5-Aza-CdR may be a potential radiosensitizer to improve the therapy effect in osteosarcoma. © International Society of Oncology and BioMarkers (ISOBM) 2014.

Chen Y.,Chinese PLA General Hospital | Yu Z.,Pla No 161 Center Hospital | Zhang B.,Shenzhen University | Chang Z.,General Hospital of Jinan Military Commanding Region | And 2 more authors.
Tumor Biology | Year: 2014

A number of studies have investigated the association between CRR9p polymorphism and risk of lung cancer (LC), yet the role in LC pathogenesis remains unclear owing to inconsistencies across studies. We searched PubMed, Embase, and Web of Science for all medical literature published until January 2014. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were obtained by means of the fixed effects model. Data from eight studies satisfying the predesigned inclusion criteria were selected for this meta-analysis. We found a statistically significant evidence for a protective effect on the overall LC risk (TT vs. CC: OR = 0.78, 95 % CI = 0.70–0.87, Phet = 0.299; TT vs. CT + CC: OR = 0.81, 95 % CI = 0.73–0.90, Phet = 0.113; T vs. C: OR = 0.90, 95 % CI = 0.86–0.95, Phet = 0.758; TT + CT vs. CC: OR = 0.92, 95 % CI = 0.87–0.98, Phet = 0.892). Both Caucasian and Asian populations were suggested to have a reduced risk of developing such cancer. In the analysis of the association between rs401681 and non-small cell lung cancer (NSCLC) risks, all of the contrast models showed similar results except the CT vs. CC genetic model (OR = 0.93, 95 % CI = 0.84–1.02, Phet = 0.568). Our meta-analysis provides supportive evidence that CRR9p polymorphism may influence a risk of LC and NSCLC in a protective model. © 2014, International Society of Oncology and BioMarkers (ISOBM).

Zhu W.,Chinese PLA General Hospital | Lu L.,Jindu Hospital | Li Y.,Chinese PLA General Hospital | Yao J.,Pla No 161 Center Hospital | Xu B.,Chinese PLA General Hospital
Tumor Biology | Year: 2014

The potentially functional polymorphism Arg72Pro in p53 gene has been implicated in glioma risk, but published studies have mixed findings. The aim of current investigation was to identify whether p53 Arg72Pro polymorphism was significantly associated with the risk of glioma. By searching the databases of PubMed, EMBASE, and Web of Science, our meta-analysis included ten eligible studies consisting of 2,645 glioma cases and 3,920 control subjects. The association between p53 Arg72Pro polymorphism and glioma risk was assessed by summarizing the odds ratios (ORs) with the corresponding 95 % confidence intervals (CIs). We found that there was no overall risk of glioma in relation to any genetic model of p53 Arg72Pro polymorphism. Similar results were implicated in the analyses which are subgrouped by ethnicity and source of controls. This nonsignificant association remained stable when analyses were restrained to the studies consistent with HWE. In conclusion, our meta-analysis, based on the combined data from published papers before May 2013, reveals no evidence for significant association between p53 Arg72Pro polymorphism and glioma risk. © 2014 International Society of Oncology and BioMarkers (ISOBM).

Zhang Q.,Chinese PLA General Hospital | Geng P.-L.,Chinese PLA General Hospital | Yin P.,Chinese PLA General Hospital | Wang X.-L.,Chinese PLA General Hospital | And 2 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2013

Objective: To investigate the expression level of TUG1 and one of its transcript variants (n377360) in osteosarcoma cells and assess the role of TUG1 in proliferation and apoptosis in the U2OS cell line. Methods: TUG1 and n377360 expression levels in patients with osteosarcomas and the U2OS human osteosarcoma cell line were evaluated using real-time quantitative PCR. U2OS cells were transected with TUG1 and n377360 siRNA or non-targeting siRNA. MTS was performed to assess the cell proliferation and flow cytometry was applied to analyze apoptosis. Results: We found significantly higher TUG1 and n377360 expression levels in osteosarcoma tissues compared with matched non-tumorous tissues. In line with this, suppression of TUG1 and n377360 expression by siRNA significantly impaired the cell proliferation potential of osteosarcoma cells. Furthermore, inhibition of TUG1 expression significantly promoted osteosarcoma cell apoptosis. Conclusions: The overexpression of TUG1 and n377360 in osteosarcoma specimens and the functional role of TUG1 and n377360 regarding cell proliferation and apoptosis in an osteosarcoma cell line provided evidence that the use of TUG1 or n377360 may be a viable but an as yet unexplored therapeutic strategy in tumors that over express these factors.

Wang Y.,Chinese PLA General Hospital | Yao J.,Pla No 161 Center Hospital | Yao J.,Chinese PLA General Hospital | Meng H.,Chinese PLA General Hospital | And 5 more authors.
Molecular Medicine Reports | Year: 2015

Long non-coding RNAs (lncRNAs) have recently been identified as novel modulators of malignant tumors. However, the function of lncRNAs in cancer stem cells (CSCs) remains to be elucidated. The present study aimed to investigate the regulating role of a novel lncRNA, hypoxia-inducible factor-2α (HIF-2α) promoter upstream transcript (HIF2PUT), in osteosarcoma stem cells. The expression levels of HIF2PUT were assessed by quantitative polymerase chain reaction in 17 osteosarcoma tissue specimens, and the correlation between the expression of HIF2PUT and its host transcript-HIF-2α was determined. In functional experiments, HIF2PUT expression was knocked down by small interfering RNAs, or overexpressed by transfection with pcDNA-HIF2PUT, in order to evaluate the effects of HIF2PUT on cell proliferation, migration, expression rate of osteosarcoma stem cell marker CD133, and stem sphere-forming ability in MG63 cells. HIF2PUT expression levels were positively correlated with HIF-2α in osteosarcoma tissues. Overexpression of HIF2PUT markedly inhibited cell proliferation and migration, decreased the percentage of CD133 expressing cells, and impaired the osteosarcoma stem sphere-forming ability of the MG63 cells. Whereas, knockdown of HIF2PUT expression had the opposite effect. Furthermore, altering the expression of HIF2PUT resulted in a concomitant change to HIF-2α mRNA expression. These results indicate that the lncRNA HIF2PUT may be a novel regulatory factor of osteosarcoma stem cells, which may exert its function partly by controlling HIF-2α expression. Further studies regarding HIF2PUT may provide a novel therapeutic target of osteosarcoma in the future.

Kong X.-P.,Chinese PLA General Hospital | Kong X.-P.,Tianjin University | Yao J.,Pla No 161 Center Hospital | Luo W.,Chinese PLA General Hospital | And 5 more authors.
Molecular and Cellular Biochemistry | Year: 2014

The Fork head box C1 (FOXC1) gene is overexpressed in multiple malignant tumors and is functionally correlated with tumor progression. However, its’ role in oral squamous cell carcinoma (OSCC) is still unclear. Recent studies have revealed that many long non-coding RNA (lncRNAs) cooperate with adjacent coding genes and form a functional “lncRNA-mRNA pair”. In this study, we report a new lncRNA FOXC1 upstream transcript (FOXCUT) that was remarkably overexpressed in 23 OSCC patients, as was the adjacent FOXC1 gene. The expressions of FOXC1 and FOXCUT were positively correlated. When the expression of FOXCUT was down-regulated by small interfering RNA (siRNA), the expression of FOXC1 was also decreased. Moreover, in OSCC cells Tca8113 and SCC-9, down-regulation of either FOXC1 or FOXCUT by siRNA could inhibit cell proliferation and cell migration in vitro and was accompanied with a reduction of MMP2, MMP7, MMP9, and VEGF-A. In conclusion, FOXC1 may be co-amplified with FOXCUT in OSCC, and both of them may be functionally involved in the tumor progression of OSCC. This provides evidence that both FOXC1 and FOXCUT may serve as novel biomarkers and therapeutic targets in OSCC patients who overexpress this “lncRNA-mRNA pair”. © 2014, The Author(s).

Geng P.,Chinese PLA General Hospital | Yao J.,Chinese PLA General Hospital | Yao J.,Pla No 161 Center Hospital | Zhu Y.,Chinese PLA General Hospital | Zhu Y.,Beijing Jiaotong University
Molecular Biology Reports | Year: 2014

The Ser326Cys polymorphism in the human 8-oxogunaine glycosylase (hOGG1) gene with lung cancer susceptibility had been investigated by the approaches of PCR-RFLP, PCR-SSCP and ASA. Due to limited specimen and different approaches the conclusion was drawn toughly. To evaluate this correlation comprehensively, a meta-analysis was performed based on 30 case-control studies, including 10,327 cases and 12,148 controls. The random-effects model was used to estimate the odds ratios and 95 % confidence interval for various contrasts of this polymorphism. The combined results suggested that the hOGG1 Ser326Cys polymorphism was not associated with lung cancer susceptibility in different genetic models. Similarly, in the stratified analyses by ethnicity and source of control, no risk was observed between all the genetic models and lung cancer risk. Our meta-analysis revealed that there was little correlation between the hOGG1 Ser326Cys polymorphism and the risk of lung cancer. © 2014 Springer Science+Business Media Dordrecht.

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