Hypoxic conditions differentially regulate TAZ and YAP in cancer cells

Libo Yan, Qingchun Cai, Yan Xu

Research output: Contribution to journalArticle

17 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)31-36
Number of pages6
JournalArchives of Biochemistry and Biophysics
Volume562
DOIs
StatePublished - Nov 15 2014

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Cells
Neoplasms
Proteins
Cell Hypoxia
Phosphorylation
Cell proliferation
Cell Movement
Carcinogenesis
Phosphotransferases
Epithelial Cells
Cell Proliferation
Cell Line
Hypoxia
Ovarian epithelial cancer

Keywords

  • Hippo-YAP pathway
  • Hypoxia
  • TAZ (transcriptional co-activator with PDZ-binding motif)
  • YAP (Yes-associated protein)

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology
  • Medicine(all)

Cite this

Hypoxic conditions differentially regulate TAZ and YAP in cancer cells. / Yan, Libo; Cai, Qingchun; Xu, Yan.

In: Archives of Biochemistry and Biophysics, Vol. 562, 15.11.2014, p. 31-36.

Research output: Contribution to journalArticle

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