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骨髓分化因子88通过核因子-κB/活化蛋白-1信号通路调控结直肠癌细胞增殖、迁移和侵袭的机制研究

Myeloid differentiation factor 88 regulates the proliferation, migration and invasion of colorectal cancer cells through the nuclear factor-κB/activator protein-1 signaling pathway

    摘要
  • 摘要:
    目的 探讨骨髓分化因子88(MyD88)在结直肠癌发生发展中的功能和潜在机制。
    方法 在SW480细胞中稳定敲低MyD88。采用CCK-8实验检测细胞的增殖能力; 采用Transwell和划痕实验检测结直肠癌细胞的迁移能力; 采用Transwell实验分析结直肠癌的侵袭能力; 采用蛋白质印迹法(Western blot)分析MyD88的潜在调控机制。
    结果 实时荧光定量聚合酶链式反应(RT-qPCR)和Western blot结果显示, 本研究在结直肠癌细胞中成功敲低了MyD88的表达。结直肠癌细胞中MyD88的降低可以显著抑制细胞的生长和侵袭。进一步研究发现，在结直肠癌细胞中敲低MyD88可以显著抑制MyD88-NF-κB/AP-1信号通路的表达。
    结论 MyD88基因在结直肠癌的发生发展中起着重要的作用，有望成为结直肠癌的潜在的诊断和预后生物标志物。

     

    Abstract:
    Objective To investigate the function and potential mechanism of myeloid differentiation factor 88 (MyD88) in the occurrence and development of colorectal cancer.
    Methods Stable knockdown of MyD88 was performed in SW480 cells. The proliferation ability of cells was detected by CCK-8 assay; the migration ability of colorectal cancer cells was examined by Transwell and scratch assay; the invasion ability of colorectal cancer was analyzed by Transwell assay; the potential regulatory mechanism of MyD88 was analyzed by Western blot.
    Results Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blot results showed successful downregulation of MyD88 expression in colorectal cancer cells. The decrease of MyD88 in colorectal cancer cells significantly inhibited cell growth and invasion. Further studies revealed that knockdown of MyD88 in colorectal cancer cells significantly inhibited the expression of the MyD88-NF-κB/AP-1 signaling pathway.
    Conclusion MyD88 gene plays an important role in the occurrence and development of colorectal cancer and may become a potential diagnostic and prognostic biomarker for colorectal cancer.

     

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