| Literature DB >> 28479254 |
Siheng Zhang1, Yutian Miao2, Xianchong Zheng2, Yong Gong3, Jinxin Zhang2, Fei Zou4, Chunqing Cai5.
Abstract
The Ca2+ sensor proteins STIM1 and STIM2 are crucial elements of store-operated calcium entry (SOCE) in breast cancer cells. Increased SOCE activity may contribute to epithelial-mesenchymal transitions (EMT) and increase cell migration and invasion. However, the roles of STIM1 and STIM2 in TGF-β-induced EMT are still unclear. In this study, we demonstrate roles of STIMs in TGF-β-induced EMT in breast cancer cells. In particular, STIM1 and STIM2 expression affected TGF-β-induced EMT by mediating SOCE in MDA-MB-231 and MCF-7 breast cancer cells. The specific SOCE inhibitor YM58483 blocked TGF-β-induced EMT, and differing effects of STIM1 and STIM2 on TGF-β-induced EMT correlated with differing roles in SOCE. Finally, we showed that STIM2 is associated with non-store-operated calcium entry (non-SOCE) during TGF-β-induced EMT, whereas STIM1 is not. What's more, non-SOCE have a large possibility to be ROCE. In conclusion, STIM1 and STIM2 proteins play important roles in TGF-β-induced EMT and these effects are related to both SOCE and non-SOCE.Entities:
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Year: 2017 PMID： 28479254 DOI： 10.1016/j.bbrc.2017.05.009
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575