Down-regulation of long noncoding RNA MEG3 promotes cell proliferation in gastric cancer
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    Abstract:

    Objective:To investigate the expression level of long noncoding RNA MEG3 in gastric cancer tissues and cell lines,and to study the effect of up-regulation of MEG3 expression on gastric cancer cells proliferation and its possible mechanisms. Methods:Quantitative reverse-transcription PCR was performed to detect the relative expression of MEG3 in gastric cancer cell lines and tissues. pcDNA-MEG3 was transfected into BGC-823 cells and MGC-803 cells to down-regulate MEG3 expression,and quantitative reverse-transcription PCR was used to test the transfection efficiency. MTT and colony formation assays were performed to detect the effect of MEG3 on gastric cancer cells proliferation. Western blot assay was used to test the expression level of p53 protein in MGC-803 cells and BGC-823 cells transfected with pcDNA-MEG3,respectively. Results:This study showed that MEG3 was lowly expressed both in gastric cancer samples and cell lines compared with their corresponding normal tissues and cell lines. The expression level of MEG3 in SGC7901,MGC-803 and BGC-823 cells were 73.6%,42.0% and 27.1% of that in normal gastric epithelium cell GES-1,respectively(P < 0.05). Transfection of pcDNA-MEG3 significantly increased its expression in BGC-823 cells and MGC-803 cells,respectively,252 and 311 folds compared with control cells(P < 0.05). MTT and colony formation assays indicated that up-regulated MEG3 inhibited BGC-823 and MGC-803 cells proliferation. Western blot assay showed that the expression level of p53 protein was significantly increased in MGC-803 cells and BGC-823 cells transfected with pcDNA-MEG3, compared with the control group,respectively. Conclusion:Down-regulated MEG3 could promote gastric cells proliferation,probably by inhibiting the activation of p53 protein,and thus affect the development and progression of gastric cancer.

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孙 倩,刘博巽,林梦洁,尹凌帝,陈志强,孙 明,德 伟,刘志军.长链非编码RNA MEG3对胃癌细胞增殖的影响[J].南京医科大学学报(自然科学版英文版),2014,(1):001-006.

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  • Received:October 12,2013
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  • Online: January 27,2014
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