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YAP enhances autophagic flux to promote breast cancer cell survival in response to nutrient deprivation.

PloS one (2015-03-27)
Qinghe Song, Beibei Mao, Jinbo Cheng, Yuhao Gao, Ke Jiang, Jun Chen, Zengqiang Yuan, Songshu Meng
RESUMEN

The Yes-associated protein (YAP), a transcriptional coactivator inactivated by the Hippo tumor suppressor pathway, functions as an oncoprotein in a variety of cancers. However, its contribution to breast cancer remains controversial. This study investigated the role of YAP in breast cancer cells under nutrient deprivation (ND). Here, we show that YAP knockdown sensitized MCF7 breast cancer cells to nutrient deprivation-induced apoptosis. Furthermore, in response to ND, YAP increased the autolysosome degradation, thereby enhancing the cellular autophagic flux in breast cancer cells. Of note, autophagy is crucial for YAP to protect MCF7 cells from apoptosis under ND conditions. In addition, the TEA domain (TEAD) family of growth-promoting transcription factors was indispensable for YAP-mediated regulation of autophagy. Collectively, our data reveal a role for YAP in promoting breast cancer cell survival upon ND stress and uncover an unappreciated function of YAP/TEAD in the regulation of autophagy.

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Sigma-Aldrich
Acid phosphatase Assay Kit, 1 kit sufficient for 1,000 assays (multiwell plates), 1 kit sufficient for 100 assays (tubes)
Sigma-Aldrich
Monoclonal Anti-TEAD4 antibody produced in mouse, clone 5H3, purified immunoglobulin, buffered aqueous solution