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将小分子抗癌药物PHA-767491和携带TRAIL基因的非复制型腺病毒(Ad-TRAIL)共同作用于肝癌细胞Bel-7404,探讨PHA-767491联合TRAIL蛋白对肝癌细胞增殖的协同抑制作用及其作用机理.MTT法检测细胞存活率,Hoechst 33342荧光检测细胞凋亡现象和流式细胞仪检测细胞凋亡水平.结果表明,PHA-767491联合Ad-TRAIL抑制Bel-7404细胞增殖的能力显著优于单一用药.Western印迹进一步分析蛋白表达水平显示,PHA-767491可以通过下调抗凋亡蛋白Mcl-1和Xiap的表达,从而显著增强TRAIL蛋白诱导Bel-7404细胞凋亡的能力;PHA-767491联合AdTRAIL处理Bel-7404细胞后,不仅Bel-7404细胞凋亡水平显著增加,并且伴随着PARP和Caspase3的大量剪切.本研究证实,PHA-767491和TRAIL的联合使用对抑制肝癌细胞Bel-7404增殖表现出了显著的协同效应,为今后癌症药物的联合治疗提供了新的思路.
The small molecule anticancer drug PHA-767491 and the TRAIL gene-carrying non-replicating adenovirus (Ad-TRAIL) act on the hepatocellular carcinoma cells Bel-7404 to investigate the synergistic inhibitory effect of PHA-767491 and TRAIL on the proliferation of hepatocellular carcinoma cells and their The mechanism of action.MTT assay of cell viability, Hoechst 33342 fluorescence detection of apoptosis and flow cytometry detection of apoptosis levels.The results showed that PHA-767491 combined with Ad-TRAIL significantly inhibited Bel-7404 cell proliferation ability The results of Western blotting showed that PHA-767491 could significantly enhance the apoptosis of Bel-7404 cells induced by TRAIL by down-regulating the expression of anti-apoptotic proteins Mcl-1 and Xiap. PHA-767491 combined with AdTRAIL After treatment of Bel-7404 cells, not only the level of apoptosis in Bel-7404 cells increased significantly, but also a large amount of cleavage of PARP and Caspase3.The study shows that the combination of PHA-767491 and TRAIL can inhibit the proliferation of Bel-7404 hepatoma cells A significant synergistic effect, for the future combination of cancer drugs provides a new way of thinking.