期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 125, 期 5, 页码 2123-2135出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI79573
关键词
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资金
- Ministry of Science and Technology of the People's Republic of China (MOST) [2015CB910401, 2011CB910601, 2012CB910103]
- National Natural Science Foundation of China (NSFC) [81430057, 81225016, 31271454]
- Shanghai Key Basic Research Program [12JC1401100]
- 100 Talents Program of Shanghai Health [XBR2011041]
- Scholar of Dawn Program of the Shanghai Education Commission
- Shanghai Outstanding Academic Leader grant [13XD1400600]
- 985 Program
- Shanghai Leading Academic Discipline Project [pB110]
- NIH grants
The G protein coupled estrogen receptor (GPER) mediates both the genomic and nongenomic effects of estrogen and has been implicated in breast cancer development. Here, we compared GPER expression in cancerous tissue and adjacent normal tissue in patients with invasive ductal carcinoma (IDC) of the breast and determined that GPER is highly upregulated in cancerous cells. Additionally, our studies revealed that GPER stimulation activates yes-associated protein 1 (YAP) and transcriptional coactivator with a PDZ-binding domain (TAZ), 2 homologous transcription coactivators and key effectors of the Hippo tumor suppressor pathway, via the G alpha q-11, PLC beta/PKC, and Rho/ROCK signaling pathways. TAZ was required for GPER-induced gene transcription, breast cancer cell proliferation and migration, and tumor growth. Moreover, TAZ expression positively correlated with GPER expression in human IDC specimens. Together, our results suggest that the Hippo/YAP/TAZ pathway is a key downstream signaling branch of GPER and plays a critical role in breast tumorigenesis.
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