| 金 一,马 特,蒋书玲.蛋白酶体抑制剂通过 Bcl-2 相关抗凋亡蛋白 3 剪切诱导乳腺癌 MCF-7 细胞凋亡[J].肿瘤学杂志,2014,20(2):81-85. |
| 蛋白酶体抑制剂通过 Bcl-2 相关抗凋亡蛋白 3 剪切诱导乳腺癌 MCF-7 细胞凋亡 |
| Proteasome Inhibitor Induced Apoptosis in MCF-7 Breast Cancer Cells Through Cleavage of BAG3 Protein |
| 投稿时间：2013-09-26 |
| DOI：10.11735/j.issn.1671-170X.2014.02.B001 |
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| 中文关键词: 胱天蛋白酶 Bcl-2相关抗凋亡基因3 蛋白酶体抑制剂 乳腺肿瘤 |
| 英文关键词:caspase Bcl-2-associated athanogene 3 proteasome inhibitor breast neoplasms |
| 基金项目:沈阳市科技局科学技术研究项目（P120552） |
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| 摘要点击次数: 1922 |
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| 中文摘要: |
| 摘 要：［目的］ 探讨蛋白酶体抑制剂诱导乳腺癌MCF-7细胞凋亡与BAG3蛋白剪切的相互关系，以及BAG3蛋白剪切是否依赖胱天蛋白酶介导完成。［方法］ 选取人MCF-7乳腺癌细胞系，设空白对照组、MG132处理组、Z-VAD处理组和MG132+Z-VAD联合组。实时定量RT-PCR和Western Blot分别检测各组细胞中BAG3 mRNA和蛋白的表达水平；流式细胞仪检测细胞凋亡。［结果］ MG132诱导乳腺癌细胞凋亡过程中BAG3基因和蛋白表达均增高(P<0.05)，但BAG3蛋白剪切体也随之增加，流式细胞术结果证明细胞凋亡率增高(P<0.05)。同时，应用胱天蛋白酶体抑制剂Z-VAD处理细胞后，BAG3蛋白剪切体消失。［结论］ 蛋白酶体抑制剂可诱导上调乳腺癌MCF-7细胞中BAG3基因和蛋白的表达，但BAG3蛋白裂解增强，可导致细胞凋亡增加，这一效应可能依赖胱天蛋白酶介导完成。 |
| 英文摘要: |
| Abstract：［Purpose］ To investigate the role of BAG3 in proteasome inhibitor mediated apoptosis in breast cancer MCF-7 cells and whether BAG3 was cleaved in a caspase-dependent manner. ［Methods］ MCF-7 cell was cultured and treated with vehicle，MG132，pancaspase inhibitor Z-VAD or combination of Z-VAD and MG132． BAG3 mRNA and protein levels were analyzed by RT-PCR and Western Blot respectively．Flow cytometry(FCM) was used to determine the apoptotic rate of cells.［Results］ Western Blot and Real-time PCR showed that both mRNA and protein expressions of BAG3 in the cells increased by MG132 treatment(P<0.05) and cleavage product of BAG3 was also induced by MG132，accompanied with increasing apoptosis rate(P<0.05). Cleavage of BAG3 was inhibited by caspase inhibitor Z-VAD.［Conclusion］ Proteasome inhibitor could induce the up-regulation of BAG3 mRNA and protein in MCF-7 cells，but the enhanced proteolytic cleavage of BAG3 could be contribute to increasement of apoptosis，whose process might be mediated in a caspase-dependent manner. |
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