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目的:探讨ERK/FoxO3a信号轴是否介导牡荆脂素(VB-1)对人肝癌HepG2细胞系增殖的抑制作用。方法:MTT法观察不同浓度VB-1对人肝癌HepG2细胞系和永生化人胚肝L-02细胞系增殖的影响,集落形成法检测细胞生长,Western blot检测ERK1/2,FoxO3a蛋白磷酸化水平。结果:VB-1以浓度依赖方式抑制HepG2细胞增殖活性,对L-02细胞作用微弱。VB-1有效抑制HepG2细胞锚定依赖生长,并降低p-ERK1/2,p-FoxO3a表达水平,呈浓度依赖性。MEK抑制剂PD98059增强VB-1抑制HepG2细胞增殖和ERK1/2,FoxO3a磷酸化的作用。结论:VB-1通过阻断ERK/FoxO3a信号轴抑制肝癌HepG2细胞增殖活性。
OBJECTIVE: To investigate whether ERK / FoxO3a signal axis can mediate the inhibitory effect of Vitexin (VB-1) on the proliferation of human hepatoma HepG2 cell line. Methods: MTT assay was used to observe the effects of different concentrations of VB-1 on the proliferation of human hepatoma HepG2 cells and immortalized human embryonic liver L-02 cells. The cell growth was detected by colony formation assay. The levels of phosphorylated ERK1 / 2 and FoxO3a . Results: VB-1 inhibited the proliferation of HepG2 cells in a concentration-dependent manner and had a weak effect on L-02 cells. VB-1 effectively inhibited the anchorage-dependent growth of HepG2 cells and decreased the expression of p-ERK1 / 2 and p-FoxO3a in a concentration-dependent manner. MEK inhibitor PD98059 enhanced the inhibitory effect of VB-1 on HepG2 cell proliferation and ERK1 / 2, FoxO3a phosphorylation. Conclusion: VB-1 can inhibit the proliferation of HepG2 cells by blocking the signal of ERK / FoxO3a.