SAHA影响乳腺癌MCF-7细胞增殖的分子机制研究  

Molecular Mechanisms of SAHA Inhibiting the Proliferation of MCF-7 Breast Cancer Cells

作　　者：刘春阳 周伟强[2] LIU Chunyan;Weiqiang Zhou(Grade 2016,Shenyang Medical College,Shenyang 110034,China;Shenyang Medical College,Key Laboratory of Environmental Pollution and Microecology of Liaoning Province)

机构地区：[1]沈阳医学院基础医学院,辽宁沈阳110034 [2]沈阳医学院基础医学院,辽宁省环境污染与微生态重点实验室

出　　处：《沈阳医学院学报》2018年第4期370-372,共3页Journal of Shenyang Medical College

基　　金：国家自然科学基金项目(No.81172509);辽宁省大学生创新创业科研基金项目(No.201710164000013)

摘　　要：目的:研究组蛋白去乙酰化酶抑制剂SAHA抑制乳腺癌MCF-7细胞增殖的分子机制。方法:采用固相细胞凋亡抗体芯片技术测定SAHA对MCF-7细胞周期调控蛋白及细胞凋亡蛋白表达的影响。结果:与空白对照组比较,SAHA显著增强MCF-7细胞中调控细胞周期G1-S期的p21CIP1和p27KIP1蛋白的表达水平,并抑制Survivin蛋白的表达;增加细胞凋亡相关蛋白Bax、TRAIL DR5和Capase-3的表达水平,降低Claspin、Clusterin和XIAP的表达水平,差异均有统计学意义(P<0.05)。结论:SAHA通过调控细胞周期调控蛋白和细胞凋亡蛋白的表达而达到抑制乳腺癌细胞增殖的目的。Objective:To study the molecular mechanisms of SAHA inhibiting the cell proliferation of MCF-7 breast cancer cells.Methods:Apoptotic antibody microarray array was used to determine the effects of SAHA on the expression of cell-cycle associated proteins and apoptotic proteins.Results:Compared with control group,SAHA significantly increased the expression levels of p21CIP1 and p27KIP1,and inhibited Survivin production(P<0.05).SAHA also increased the expression levels of Bax,TRAIL DR5 and Capase-3,and decreased the expression levels of Claspin,Clusterin and XIAP significantly(P<0.05).Conclusion:By regulating the expression of cell-cycle associated proteins and apoptotic proteins,SAHA inhibits the cell cycle progression in MCF-7 cells.

关 键 词：乳腺癌 MCF-7细胞 SAHA 

分 类 号：R394.3[医药卫生—医学遗传学]