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首页|YAP Enhances Autophagic Flux to Promote Breast Cancer Cell Survival in Response to Nutrient Deprivation

YAP Enhances Autophagic Flux to Promote Breast Cancer Cell Survival in Response to Nutrient Deprivation

中文摘要英文摘要

he 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.

he 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.

Cheng, Jinbo、Jiang, Ke、Gao, Yuhao、Song, Qinghe、Chen, Jun、Meng, Songshu、Mao, Beibei、Yuan, Zengqiang、Song, Qinghe、Gao, Yuhao、Yuan, Zengqiang

10.12074/201605.01499V1

肿瘤学细胞生物学分子生物学

HIPPO SIGNALING PATHWAYINHIBITS AUTOPHAGYHETEROZYGOSITYPOPTOSISPROTEINPROLIFERATIONEATHIDENTIFICATIONUMORIGENESIS

Cheng, Jinbo,Jiang, Ke,Gao, Yuhao,Song, Qinghe,Chen, Jun,Meng, Songshu,Mao, Beibei,Yuan, Zengqiang,Song, Qinghe,Gao, Yuhao,Yuan, Zengqiang.YAP Enhances Autophagic Flux to Promote Breast Cancer Cell Survival in Response to Nutrient Deprivation[EB/OL].(2016-05-12)[2025-08-02].https://chinaxiv.org/abs/201605.01499.点此复制

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