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目的 研究3种化疗药物抑制肝癌SMMC-7721细胞增殖、促进细胞凋亡过程中端粒酶活性及细胞外调节蛋白激酶（ERK）磷酸化蛋白表达水平的变化,探讨端粒酶与ERK在肝癌细胞凋亡过程中的调节作用及相互之间的关系。方法 用MTT法、流式细胞术检测法、端粒重复序列扩增法（TRAP法）、生物发光分析法及western blot检测法。结果3种化疗药物使肝癌细胞增殖受抑（抑制率分别为:028％±0.08％、0.25％±0.16％和0.24％±0.11％）并诱发凋亡（凋亡率分别为21.12％、28.83％和12.30％）的同时,端粒酶活性也有不同程度减低（分别为对照组的46％、65％和98％）;处于活化状态的磷酸化ERK1/2蛋白表达水平下降。结论ERK通路可能是化疗药物下调端粒酶活性,进而促进细胞凋亡的机制之一。
Objective To investigate the changes of telomerase activity and phosphorylated ERK protein expression in three hepatocellular carcinoma cell lines SMMC-7721 in vitro and in vitro, Apoptosis in the regulatory role and the relationship between each other. Methods MTT assay, flow cytometry assay, telomeric repeat amplification (TRAP) assay, bioluminescence assay and western blot were used. Results The three chemotherapeutic drugs inhibited the proliferation of hepatoma cells (the inhibitory rates were 028% ± 0.08%, 0.25% ± 0.16% and 0.24% ± 0.11%, respectively) and induced apoptosis (apoptosis rates were 21.12% and 28.83% And 12.30%, respectively), telomerase activity was reduced to some extent (46%, 65% and 98% of the control group, respectively). The expression of phosphorylated ERK1 / 2 in the activated state was decreased. Conclusion ERK pathway may be one of the mechanisms by which chemotherapeutic drugs down-regulate telomerase activity and promote apoptosis.