| Literature DB >> 25234598 |
Jie Li1, Xi-fei Yang2, Xiao-hu Ren1, Xiao-jing Meng3, Hai-yan Huang2, Qiong-hui Zhao4, Jian-hui Yuan2, Wen-xu Hong2, Bo Xia2, Xin-feng Huang2, Li Zhou2, Jian-jun Liu5, Fei Zou6.
Abstract
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.Entities:
Keywords: Breast cancer; MMP-9; PP2Ac; RNAi; SET
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Year: 2014 PMID: 25234598 DOI: 10.1016/j.bbrc.2014.09.013
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575