Tian Yao, Yu Yue, Hou Li-Kun, Chi Jiang-Rui, Mao Jie-Fei, Xia Li, Wang Xin, Wang Ping, Cao Xu-Chen
The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
Cancer Sci. 2016 Mar;107(3):274-80. doi: 10.1111/cas.12879. Epub 2016 Feb 13.
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.
血清剥夺反应蛋白（SDPR）是蛋白激酶C的关键底物，在诱导膜曲率以及参与小窝的形成过程中发挥着关键作用。然而，SDPR在癌症发生和发展中的功能仍不清楚。在此，我们发现SDPR在人类乳腺癌中表达下调。SDPR的过表达抑制MDA-MB-231细胞的增殖和侵袭，而SDPR的缺失则促进MCF10A细胞的增殖和侵袭。随后，SDPR的缺失诱导上皮-间质转化（EMT）样表型。最后，SDPR的敲低通过上调TGF-β1的表达激活转化生长因子-β（TGF-β）信号通路。总之，我们的结果表明，SDPR通过阻断TGF-β信号通路抑制乳腺癌进展。血清剥夺反应蛋白抑制乳腺癌细胞的增殖和侵袭。SDPR的缺失通过激活TGF-β信号通路诱导上皮-间质转化。
