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目的:探讨力达霉素(lidamycin,LDM)诱导人肝癌BEL-7402和正常人肝L-02细胞出现的有丝分裂性细胞死亡的差异。方法:采用MTT法观察LDM对BEL-7402和L-02细胞生长曲线的影响;使用Gi-emsa染色和流式细胞术观察有丝分裂性细胞死亡特征;用Western blot法检测蛋白表达变化。结果:LDM抑制BEL-7402和L-02细胞的生长,二者均表现出有丝分裂性细胞死亡的特征,即细胞体积增大、G2/M期阻滞、出现多核化,但BEL-7402细胞对LDM更敏感。在LDM处理的BEL-7402和L-02细胞中,与凋亡相关的Bax和Smac的蛋白表达水平没有增加,caspase-3和caspase-9未被活化,但L-02细胞的Akt通路被激活。结论:人正常L-02细胞对LDM引起的有丝分裂性细胞死亡明显低于人肝癌BEL-7402细胞,对LDM的反应敏感性存在差异的原因可能与Akt信号通路有关。
AIM: To investigate the differences of mitotic cell death in lidamycin (LDM) -induced liver cancer BEL-7402 and normal human L-02 cells. Methods: The effects of LDM on the growth curve of BEL-7402 and L-02 cells were observed by MTT assay. The characteristics of mitotic cell death were observed by Gi-emsa staining and flow cytometry. The protein expression was detected by Western blot. RESULTS: LDM inhibited the growth of BEL-7402 and L-02 cells, both of which showed the characteristics of mitotic cell death, ie cell volume increased, G2 / M phase arrest, and multinucleation, but BEL-7402 cell pair LDM more sensitive. In LDM-treated BEL-7402 and L-02 cells, the expression of apoptosis-related Bax and Smac protein did not increase, while caspase-3 and caspase-9 were not activated, but Akt pathway in L-02 cells was activated . CONCLUSION: LD-induced mitochondrial cell death in human normal L-02 cells is significantly lower than that in human hepatocellular carcinoma BEL-7402 cells. The difference in sensitivity to LDM may be related to the Akt signaling pathway.