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Hypoxic conditions differentially regulate TAZ and YAP in cancer cells.

Authors
  • Yan, Libo1
  • Cai, Qingchun1
  • Xu, Yan2
  • 1 Department of Obstetrics and Gynecology, Indiana University School of Medicine, 975 W. Walnut St. IB355A, Indianapolis, IN 46202, United States. , (India)
  • 2 Department of Obstetrics and Gynecology, Indiana University School of Medicine, 975 W. Walnut St. IB355A, Indianapolis, IN 46202, United States. Electronic address: [email protected] , (India)
Type
Published Article
Journal
Archives of Biochemistry and Biophysics
Publisher
Elsevier
Publication Date
Nov 15, 2014
Volume
562
Pages
31–36
Identifiers
DOI: 10.1016/j.abb.2014.07.024
PMID: 25078107
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The Hippo-YAP pathway is altered and implicated as an oncogenic signaling pathway in many human cancers. Hypoxia is an important microenvironmental factor that promotes tumorigenesis. However, the effects of hypoxia on the two most important Hippo-YAP effectors, YAP (Yes-associated protein) and TAZ (transcriptional co-activator with PDZ-binding motif), have not been reported. In this work, we demonstrated that TAZ was functionally involved in cell proliferation and/or migration in epithelial ovarian cancer (EOC) or human ovarian surface epithelial (HOSE) cells. Hypoxic conditions (1% O2 or hypoxia mimics) induced a reduction of YAP phosphorylation (S127) and total YAP expression in EOC cell lines OVCAR5 and SKOV3. However, these conditions up-regulated levels of S69 phosphorylated TAZ in EOC cells. The known TAZ kinases, Lats1 and Akt, were unlikely to be involved in up-regulated pTAZ by hypoxic conditions. Together, our data revealed new and differential regulating mechanisms of TAZ and YAP in cancer cells by hypoxia conditions. Copyright © 2014 Elsevier Inc. All rights reserved.

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