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目的探讨二氯乙酸盐(dichloroacetate,DCA)对宫颈癌细胞增殖、凋亡的影响及其可能机制。方法采用CCK-8法检测DCA对宫颈癌He La细胞增殖的影响;流式细胞仪检测DCA对He La细胞凋亡的影响;Western blot检测DCA对He La细胞凋亡相关蛋白PARP(poly ADP-ribose polymerase)和Mcl-1(myeloid cell leukemia-1)水平的影响。结果与对照组比较,DCA处理可显著抑制He La细胞增殖(P<0.01)、促进细胞凋亡(P<0.01)、升高剪切型PARP(cleaved PARP)蛋白的水平、下调凋亡抑制蛋白Mcl-1的表达。DCA对He La细胞Mcl-1蛋白的下调作用可被蛋白酶体抑制剂MG132所抑制,但不能被蛋白翻译抑制剂放线菌酮(cycloheximide,CHX)所抑制。结论 DCA促进宫颈癌细胞凋亡的作用可能与其促进蛋白酶体降解Mcl-1有关。
Objective To investigate the effects of dichloroacetate (DCA) on proliferation and apoptosis of cervical cancer cells and its possible mechanism. Methods The effect of DCA on the proliferation of cervical cancer HeLa cells was detected by CCK-8 assay. The effect of DCA on the apoptosis of HeLa cells was detected by flow cytometry. The effect of DCA on the expression of poly ADP- ribose polymerase and myeloid cell leukemia-1. Results Compared with the control group, DCA treatment significantly inhibited the proliferation of HeLa cells (P <0.01), promoted the apoptosis of cells (P <0.01), increased the cleaved PARP protein level and downregulated the expression of apoptosis inhibitor protein Mcl-1 expression. The downregulation of Mcl-1 protein in HeLa cells by DCA can be inhibited by the proteasome inhibitor MG132 but not by cycloheximide (CHX), a protein translation inhibitor. Conclusions The effect of DCA on apoptosis of cervical cancer cells may be related to the promotion of proteasome degradation of Mcl-1.