Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor‐β signaling. Issue 3 (13th February 2016)

• Record Type: Journal Article
• Authors: Tian, Yao; Yu, Yue; Hou, Li‐Kun; Chi, Jiang‐Rui; Mao, Jie‐Fei; Xia, Li; Wang, Xin; Wang, Ping; Cao, Xu‐Chen
• Is Part Of: Cancer science. Volume 107:Issue 3(2016)
• Page Start: 274
• Page End: 280
• Publication Date: 2016-02-13
• Subjects: Breast cancer -- epithelial–mesenchymal transition -- progression -- serum deprivation response -- transforming growth factor‐β; Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.12879
• Languages: English
• ISSNs: 1347-9032

Abstract

Abstract : Serum deprivation response (SDPR), a key substrate for protein kinase C, play a critical role in inducing membrane curvature and participate in the formation of caveolae. However, the function of SDPR in cancer development and progression is still not clear. Here, we found that SDPR is downregulated in human breast cancer. Overexpression of SDPR suppresses cell proliferation and invasion in MDA‐MB‐231 cells, while depletion of SDPR promotes cell proliferation and invasion in MCF10A cells. Subsequently, SDPR depletion induces epithelial–mesenchymal transition (EMT)‐like phenotype. Finally, knockdown of SDPR activates transforming growth factor‐β (TGF‐β) signaling by upregulation of TGF‐β1 expression. In conclusion, our results showed that SDPR inhibits breast cancer progression by blocking TGF‐β signaling. Serum deprivation response suppresses cell proliferation and invasion in breast cancer cells. SDPR depletion induces epithelial–mesenchymal transition by activation of TGF‐β signaling. Abstract : SDPR suppresses cell proliferation and invasion in breast cancer cells. SDPR depletion induces epithelial‐mesenchymal transition by activation of TGF‐β signaling.