CIP2A在三阴性乳腺癌中的表达及作用机制研究  

Research on the Expression of CIP2A in Human Triple Negative Breast Cancer and Its Mechanism

作　　者：张亮[1] 黄秋月[1,2] 王配军[1] 肖香玲 段超[1,2] 范春生[1] 刘莹[1] 

机构地区：[1]湖北医药学院基础医学院,湖北十堰442000 [2]湖北医药学院生物医学工程学院,湖北十堰442000

出　　处：《湖北医药学院学报》2016年第4期333-337,341,共6页Journal of Hubei University of Medicine

基　　金：2014年度湖北医药学院优秀中青年科技创新团队资助计划项目(2014CXX05);湖北医药学院2015年度研究生启动基金资助计划项目(2015QDJZR16);2016年大学生创新创业训练计划项目(201610929001)

摘　　要：目的:探讨癌抑制蛋白磷酸酶2A(cancerous inhibitor of protein phosphatase 2A,CIP2A)在三阴性乳腺癌(triple negative breast cancer,TNBC)中的生物学功能。方法:用Western blot法、实时荧光定量PCR法检测CIP2A在三阴性乳腺癌细胞中的表达情况;siRNA干扰技术转染TNBC细胞系,检测转染后TNBC细胞的增殖、侵袭能力的变化及Akt/m TOR/P70S6K信号通路蛋白的表达情况。结果:CIP2A在TNBC细胞系中的表达较低浸润性乳腺癌细胞高;敲除TNBC细胞系中CIP2A,可抑制增殖,诱发细胞凋亡和自噬;还可抑制细胞侵袭和转移;并且能抑制Akt/m TOR/P70S6K信号通路活化。结论:CIP2A是一种参与肿瘤侵袭的癌蛋白,本课题研究为CIP2A作为三阴性乳腺癌的治疗靶点提供研究基础。Objective To investigate the biological function of cancerous inhibitor of protein phosphatase 2A（ CIP2A） in human triple negative breast cancer（ TNBC）.Methods The expression of CIP2 A in TNBC cells was determined by Western blot analysis and real-time quantitative PCR（ QPCR）; siRNA was used for transfecting TNBC cells and then to detect the variation of invasiveness in the cells being transfected. The expression of Akt/m TOR/P70S6 K pathway proteins was determined by Western blot. Results The expression of CIP2 A in TNBC cell line was higher than that in low invasive breast cancer cells.After knocking out the CIP2 A gene,the proliferation,invasion and metastasis of TNB cells were inhibited but the apoptosis and autophagy were induced. Meanwhile,the activation of Akt/m TOR/P70S6 K signal pathway was inhibited.Conclusion These results validated the role of CIP2 A as an invasion relevant oncoprotein and establish CIP2 A as a promising therapeutic target of TNBC.

关 键 词：CIP2A 三阴性乳腺癌 增殖 侵袭 自噬 

分 类 号：R737.9[医药卫生—肿瘤]