Stable SET knockdown in breast cell carcinoma inhibits cell migration and invasion

被引:17
作者
Li, Jie [1 ,2 ]
Yang, Xi-fei [2 ]
Ren, Xiao-hu [1 ,2 ]
Meng, Xiao-jing [1 ]
Huang, Hai-yan [2 ]
Zhao, Qiong-hui [3 ]
Yuan, Jian-hui [2 ]
Hong, Wen-xu [2 ]
Xia, Bo [2 ]
Huang, Xin-feng [2 ]
Zhou, Li [2 ]
Liu, Jian-jun [2 ]
Zou, Fei [1 ]
机构
[1] Southern Med Univ, Sch Publ Hlth & Trop Med, Dept Occupat Hlth & Occupat Med, Guangzhou 510515, Guangdong, Peoples R China
[2] Shenzhen Ctr Dis Control & Prevent, Key Lab Modern Toxicol Shenzhen, Shenzhen 518055, Guangdong, Peoples R China
[3] Shenzhen Entry Exit Inspect & Quarantine Bur, Shenzhen, Peoples R China
基金
美国国家科学基金会;
关键词
SET; RNAi; MMP-9; PP2Ac; Breast cancer; PROTEIN PHOSPHATASE 2A; TUMOR-SUPPRESSOR PP2A; IN-VITRO; CANCER; ONCOPROTEIN; EXPRESSION; TRICHLOROETHYLENE; PHOSPHORYLATION; ACTIVATION; APOPTOSIS;
D O I
10.1016/j.bbrc.2014.09.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Breast cancer is the most malignant tumor for women, however, the mechanisms underlying this devastating disease remain unclear. SET is an endogenous inhibitor of protein phosphatase 2A (PP2A) and involved in many physiological and pathological processes. SET could promote the occurrence of tumor through inhibiting PP2A. In this study, we explore the role of SET in the migration and invasion of breast cancer cells MDA-MB-231 and ZR-75-30. The stable suppression of SET expression through lentivirus-mediated RNA interference (RNAi) was shown to inhibit the growth, migration and invasion of breast cancer cells. Knockdown of SET increases the activity and expression of PP2Ac and decrease the expression of matrix metalloproteinase 9 (MMP-9). These data demonstrate that SET may be involved in the pathogenic processes of breast cancer, indicating that SET can serve as a potential therapeutic target for the treatment of breast cancer. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:7 / 12
页数:6
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