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人接头蛋白LNK对非小细胞肺癌细胞增殖和侵袭能力的影响

Effects of human adaptor protein LNK on proliferation and invasion ability of non-small cell lung cancer cells

    摘要
  • 摘要:
    目的 探讨人接头蛋白LNK(hLNK)对非小细胞肺癌(NSCLC)发生发展的影响。
    方法 构建稳定过表达hLNK的人NSCLC细胞株H1299-hLNK及对照细胞株H1299-pCDH。采用Western blot验证上述稳转细胞株中hLNK的表达水平; 采用平板克隆实验分析hLNK过表达对H1299细胞增殖的影响; 采用划痕实验分析hLNK过表达对H1299细胞侵袭能力的影响; 对细胞中上皮间质转化(EMT)的典型标志蛋白进行分析。
    结果 成功构建过表达hLNK的人NSCLC细胞株H1299-hLNK。与对照细胞H1299-pCDH比较, hLNK过表达抑制了H1299细胞的增殖和迁移能力, 且细胞EMT水平被抑制，差异有统计学意义(P < 0.05)。
    结论 hLNK主要通过下调NSCLC细胞H1299的EMT水平抑制癌细胞的增殖、迁移。

     

    Abstract:
    Objective To investigate the effect of human adaptor protein LNK (hLNK) on the occurrence and development of non-small cell lung cancer (NSCLC).
    Methods Human NSCLC cell line H1299-hLNK with stable overexpression of hLNK and control cell line H1299-pCDH were constructed. Western blot was used to verify the expression level of hLNK in the above stable cell lines; the effect of hLNK overexpression on the proliferation of H1299 cells was analyzed by plate cloning; the effect of hLNK overexpression on the invasion ability of H1299 cells was analyzed by scratch assay; the typical marker proteins of epithelial interstitial transition (EMT) in cells were analyzed.
    Results Human NSCLC cell line H1299-hLNK overexpressed with hLNK was successfully constructed. Compared with control cells H1299-pCDH, hLNK overexpression significantly inhibited the proliferation and migration of H1299 cells, and the EMT level of H1299 cells was significantly inhibited (P < 0.05).
    Conclusion The hLNK can inhibit the proliferation and migration of cancer cells mainly by down-regulating the EMT level of NSCLC cell H1299.

     

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