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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的增殖和侵袭

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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通过促进肿瘤细胞的增殖,侵袭和转移,在调节肿瘤的发病机理和进程中起着重要作用。为了探讨miR-196b对胃癌细胞增殖和侵袭能力的影响及其机制,本研究构建了慢病毒表达载体miR-196b并转染到人胃癌细胞系MKN28中。观察miR-196b表达上调后细胞的增殖和侵袭能力,并分析PI3K / AKT / mTOR蛋白和mRNA的表达。 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)结果表明,miR-196b表达上调后MKN28细胞的增殖显着增加(P <0.01)。流式细胞仪分析表明,miR-196b降低了GO / G1期的细胞比例,但增加了S和G2期的细胞比例(P <0.05)。此外,miR-196b表达上调后,细胞克隆的形成和跨膜速率增加(P <0.01)。裸鼠肿瘤生长测试表明,miR-196b表达上调后,肿瘤生长更加迅速。随着miR-196b表达的上调,PI3K / AKT / mTOR蛋白和mRNA的表达增加。我们得出的结论是,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。

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