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首页> 外文期刊>Oncology letters >miR-196b regulates gastric cancer cell proliferation and invasion via PI3K/AKT/mTOR signaling pathway
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miR-196b regulates gastric cancer cell proliferation and invasion via PI3K/AKT/mTOR signaling pathway

机译:MIR-196B通过PI3K / AKT / MTOR信号通路调节胃癌细胞增殖和侵袭

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摘要

miR-196b plays a significant role in the regulation of tumor pathogenesis and progression by promoting tumor cell proliferation, invasion and metastasis. In order to explore the effects of miR-196b on the proliferation and invasion ability of gastric cancer cells and the involved mechanisms, in the present study the lentivirus expression vector miR-196b was constructed and transfected into the human gastric cancer cell line MKN28. The cell proliferation and invasion ability were observed and the expression of PI3K/AKT/mTOR protein and mRNA were analyzed following upregulation of the expression of miR-196b. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) results revealed that the proliferation of MKN28 cells was notably increased following upregulation of the expression of miR-196b (P<0.01). Flow cytometry analysis demonstrated that miR-196b decreased the ratios of cells in the GO/G1 stage but increased the ratios in S and G2 stage (P<0.05). Furthermore, the cell clone formation and trans-membrane rates were increased following upregulation of the expression of miR-196b (P<0.01). The nude mouse tumor growth test revealed that tumor growth was more rapid following upregulation of the expression of miR-196b. The expression of PI3K/AKT/mTOR protein and mRNA were increased following upregulation of the expression of miR-196b. We concluded that upregulation of miR-196b promotes the proliferation and invasion ability of gastric cancer cells by regulating the PI3K/AKT/mTOR pathway.
机译:MIR-196B通过促进肿瘤细胞增殖,侵袭和转移来对肿瘤发病机制和进展的调节起着重要作用。为了探讨miR-196b对胃癌细胞的增殖和侵袭能力和涉及机制的影响,在本研究中,将慢病毒表达载体miR-196b构建并转染到人胃癌细胞系MKN28中。观察到细胞增殖和侵袭能力,并在上调miR-196b表达后分析pi3k / akt / mtor蛋白和mRNA的表达。 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑鎓溴化物(MTT)结果表明,随着MIR-196b表达的上调(P <0.01)的上调,MKN28细胞的增殖显着增加。流式细胞术分析证明MIR-196B在GO / G1阶段中的细胞比率降低,但增加了S和G2阶段的比率(P <0.05)。此外,随着miR-196b表达的上调(p <0.01)的上调,增加了细胞克隆形成和跨膜速率。裸鼠肿瘤生长试验显示,随着miR-196b的表达,肿瘤生长越来越快。在miR-196b表达的上调后增加了PI3k / akt / mTOR蛋白和mRNA的表达。我们得出结论,MIR-196B的上调通过调节PI3K / AKT / MTOR途径来促进胃癌细胞的增殖和侵袭能力。

著录项

  • 来源
    《Oncology letters 》 |2016年第1期| 共5页
  • 作者单位

    Wuhan Univ Renmin Hosp Dept Oncol 99 Zhangzhidong Wuhan 430060 Hubei Peoples R China;

    PLA Hosp 281 Dept Gastroenterol Qinhuangdao 066100 Hubei Peoples R China;

    Wuhan Univ Renmin Hosp Dept Oncol 99 Zhangzhidong Wuhan 430060 Hubei Peoples R China;

    Wuhan Univ Renmin Hosp Dept Oncol 99 Zhangzhidong Wuhan 430060 Hubei Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学 ;
  • 关键词

    miR-196b; gastric cancer; proliferation; invasion; PI3K; AKT; mTOR;

    机译:mir-196b;胃癌;增殖;入侵;pi3k;akt;mtor;

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