EBV裂解期基因BZLF1通过MAPK通路调控肺癌细胞增殖的作用研究

    Study on the Role of EBV Lytic Phase Gene BZLF1 in Regulating the Proliferation of Lung Cancer Cells Through the MAPK Pathway

    • 摘要:
      目的 探究EB病毒(Epstein-Barr virus,EBV)裂解期基因BZLF1在肺癌细胞中对细胞增殖的调节机制,旨在阐明EBV裂解期基因在肺癌细胞的作用机制。
      方法 通过构建外源性慢病毒稳转株,以人肺癌细胞株转染空载为对照组,在肺癌细胞系中过表达BZLF1并用嘌呤霉素进行筛选。将构建成功的细胞模型进行克隆形成、Transwell迁移和划痕实验等表型实验观察BZLF1对肺癌细胞的表型影响。通过流式细胞术检测过表达细胞株的细胞周期改变,通过Western blot检测MAPK信号通路变化情况。
      结果 外源性过表达BZLF1后,肺癌细胞增殖能力、迁移能力减弱,细胞周期停滞在G0/G1期,肺癌细胞中p-ERK和Cyclin D1表达水平显著下调。
      结论 EBV裂解期基因BZLF1下调p-ERK和Cyclin D1蛋白表达抑制肺癌细胞增殖能力,为进一步阐明EBV裂解期基因在肺癌细胞中的作用机制提供初步实验证据。

       

      Abstract:
      Objective To investigate the regulatory mechanism of Epstein-Barr virus (EBV) lytic gene BZLF1 on cell proliferation in lung cancer cells, and to provide experimental evidence for to clarify the mechanism of the EBV lytic phase gene in lung cancer cells.
      Methods By constructing an exogenous lentiviral stable strain of BZLF1, human lung cancer cell lines transfected with empty vector were used as the control group, and BZLF1 was overexpressed in lung cancer cells and screened by puromycin. The cell model was constructed to observe the phenotypic effect of BZLF1 on lung cancer cells by colony formation, transwell migration and scratch test. The changes of cell cycle and MAPK signaling pathway were detected by flow cytometry and western blot, respectively.
      Results After exogenous overexpression of BZLF1, the proliferation and migration ability of lung cancer cells were decreased, the cell cycle was arrested at G0/G1 phase, and the expression levels of p-ERK and Cyclin D1 were significantly down-regulated.
      Conclusions BZLF1, a lytic phase gene of EBV, inhibits the proliferation of lung cancer cells by down-regulating the expression of p-ERK and Cyclin D1, which provides preliminary experimental evidence for further elucidating the mechanism of EBV lytic phase gene in lung cancer cells.

       

    /

    返回文章
    返回