YAP Induces High-Grade Serous Carcinoma in Fallopian Tube Secretory Epithelial Cells
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Author
Hua, Guohua
Lv, Xiangmin
He, Chunbo
Remmenga, Steven W.
Rodabough, Kerry J.
Dong, Jixin
Yang, Liguo
Lele, Subodh M.
Yang, Peixin
Zhou, Jin
Karst, Alison
Drapkin, Ronny I.
Davis, John S.
Wang, Cheng
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1038/onc.2015.288Metadata
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Hua, G., X. Lv, C. He, S. W. Remmenga, K. J. Rodabough, J. Dong, L. Yang, et al. 2015. “YAP Induces High-Grade Serous Carcinoma in Fallopian Tube Secretory Epithelial Cells.” Oncogene 35 (17): 2247-2265. doi:10.1038/onc.2015.288. http://dx.doi.org/10.1038/onc.2015.288.Abstract
Accumulating evidence indicates that ovarian high-grade serous carcinoma (HGSC) originates from Fallopian tube secretory epithelial cells (FTSECs). However, the molecular mechanisms underlying the initiation and progression of HGSC derived from FTSECs remains unclear. In the present study, we found that the Hippo/YAP signaling pathway plays a critical role in the initiation and progression of Fallopian tube and ovarian HGSC. Importantly, YAP was overexpressed in inflammatory and cancerous Fallopian tube tissues. Further, overexpression of wild-type YAP, or constitutively active YAP in immortalized FTSECs, induced cell proliferation, migration, colony formation, and tumorigenesis. Moreover, the Hippo/YAP and the fibroblast growth factor (FGF) signaling pathways formed an autocrine/paracrine positive feedback loop to drive the progression of the FTSECs-derived HGSC. Evidence in this study strongly suggests that combined therapy with inhibitors of YAP (such as verteporfin) and FGFRs (such as BGJ398) can provide a novel therapeutic strategy to treat Fallopian tube and ovarian HGSC.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791205/pdf/Terms of Use
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