Endothelin Promotes Colorectal Tumorigenesis by Activating YAP/TAZ.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28249901.
- Also identified by DOI 10.1158/0008-5472.CAN-16-3229 and PMC identifier 6724531.
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Abstract
Endothelin receptor A (ETAR) promotes tumorigenesis by stimulating cell proliferation, migration, and survival. However, the mechanism of ETAR in promoting tumor growth is largely unknown. In this study, we demonstrate that ETAR stimulates colon cell proliferation, migration, and tumorigenesis through the activation of YAP/TAZ, two transcription coactivators of the Hippo tumor suppressor pathway. Endothelin-1 treatment induced YAP/TAZ dephosphorylation, nuclear accumulation, and transcriptional activation in multiple colon cancer cells. ETAR stimulation acted via downstream G-protein Gαq/11 and Rho GTPase to suppress the Hippo pathway, thus leading to YAP/TAZ activation, which was required for ETAR-induced tumorigenesis. Overall, these results indicate a critical role of the YAP/TAZ axis in ETAR signaling. <i>Cancer Res; 77(9); 2413-23. ©2017 AACR</i>.
Medical subject headings
- Adaptor Proteins, Signal Transducing
- Carcinogenesis
- Colonic Neoplasms
- Intracellular Signaling Peptides and Proteins
- Phosphoproteins
- Receptor, Endothelin A