Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24), a novel tubulin inhibitor, causes G2/M arrest and cell apoptosis by disrupting tubulin polymerization in human cervical and breast cancer cells.

作者： Daiying Zuo , Xuewei Jiang , Mengting Han , Jiwei Shen , Binyue Lang

DOI: 10.1016/J.TIV.2017.04.019

关键词: MCF-7 、 Cyclin-dependent kinase 1 、 Molecular biology 、 Nocodazole 、 Apoptosis 、 Cancer cell 、 Biology 、 Cell culture 、 HeLa 、 Cell cycle checkpoint

摘要: Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24) is a newly synthesized analogue of nocodazole by our group and has been found to be active for some cancer cells. However, its sensitivity different cell lines the underlying anticancer mechanism are still unclear. In this study, we proved that M-24 had strong time- dose-dependent anti-proliferative effects on human cervical HeLa cells breast carcinoma MCF-7 We demonstrated growth inhibitory in both were associated with microtubule depolymerization. Furthermore, treatment resulted cycle arrest at G2/M phase manner subsequent apoptosis induction. Western blotting analysis revealed up-regulation cyclin B1 cdc2 was related lines. addition, M-24-induced mainly mitochondria-dependent intrinsic pathway. mitochondrial death receptor conclusion, caused through disrupting assembly inducing Therefore, novel compound promising microtubule-destabilizing agent great potential therapy various malignancies especially cancers.

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Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24), a novel tubulin inhibitor, causes G2/M arrest and cell apoptosis by disrupting tubulin polymerization in human cervical and breast cancer cells.

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Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24), a novel tubulin inhibitor, causes G2/M arrest and cell apoptosis by disrupting tubulin polymerization in human cervical and breast cancer cells.

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