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为了观察化疗药物三尖杉酯碱(HRT)、长春新碱(VCR)和依托泊苷(VP-16)抑制肝癌细胞系SMMC7721和白血病细胞系K562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,应用MTT、流式细胞术、端粒重复序列扩增法(TRAP)、生物发光分析及Western印迹等方法进行了检测和分析。研究结果发现,一定浓度的化疗药物作用24小时后,可以抑制细胞增殖、诱导细胞凋亡;在同样作用条件下,端粒酶活性和磷酸化ERK1/2的表达也受到一定程度的抑制,其中以HRT的作用最明显。结论:HRT,VCR和VP-16可能是通过抑制Ras/Raf/MEK/ERK1/2信号传导通路、降低ERK活性、减少ERK1/2靶基因的转录活化、间接下调端粒酶活性这一共同的作用机制而发挥作用的;细胞凋亡是端粒持续缺失的的结果。
Vincristine (VCR) and etoposide (VP-16) inhibit the proliferation of human hepatocellular carcinoma cell line SMMC7721 and leukemia cell line K562 in order to observe the effects of chemotherapy drugs harringtonine (HRT), telomerase Activity and phosphorylation of extracellular regulated protein kinase (ERK) were detected and analyzed by MTT, flow cytometry, telomeric repeat amplification (TRAP), bioluminescence and Western blot . The results showed that after a certain concentration of chemotherapy drugs for 24 hours, they could inhibit cell proliferation and induce apoptosis; Under the same conditions, telomerase activity and phosphorylation of ERK1 / 2 were also inhibited to a certain extent, of which The role of HRT most obvious. CONCLUSION: HRT, VCR and VP-16 may play an important role in the suppression of ERK1 / 2 transcriptional activation and the downregulation of telomerase activity by inhibiting Ras / Raf / MEK / ERK1 / 2 signaling pathway, decreasing ERK activity Mechanism of action and apoptosis; apoptosis is the result of continued loss of telomeres.