2. Academic Validation
  3. TEAD transcription factors mediate the function of TAZ in cell growth and epithelial-mesenchymal transition

TEAD transcription factors mediate the function of TAZ in cell growth and epithelial-mesenchymal transition

  • J Biol Chem. 2009 May 15;284(20):13355-13362. doi: 10.1074/jbc.M900843200.
Heng Zhang 1,  Chen-Ying Liu 1,  Zheng-Yu Zha 2,  Bin Zhao 3,  Jun Yao 2,  Shimin Zhao 1,  Yue Xiong 4,  Qun-Ying Lei 5,  Kun-Liang Guan 6
Affiliations

Affiliations

  • 1 Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; School of Life Science Fudan University, Shanghai, China 200032.
  • 2 Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032.
  • 3 Department of Pharmacology and Moores Cancer Center, University of California at San Diego, La Jolla, California 92093-0815.
  • 4 Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599.
  • 5 Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; Department of Biological Chemistry, School of Medicine, Fudan University, Shanghai, China 200032. Electronic address: qlei@fudan.edu.cn.
  • 6 Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; Department of Pharmacology and Moores Cancer Center, University of California at San Diego, La Jolla, California 92093-0815; Department of Biological Chemistry, School of Medicine, Fudan University, Shanghai, China 200032. Electronic address: kuguan@ucsd.edu.
PMID: 19324877 DOI: 10.1074/jbc.M900843200
Abstract

The TAZ transcription co-activator has been shown to promote cell proliferation and to induce epithelial-mesenchymal transition. Recently we have demonstrated that TAZ is phosphorylated and inhibited by the Hippo tumor suppressor pathway, which is altered in human Cancer. The mechanism of TAZ-mediated transcription is unclear. We demonstrate here that TEAD is a key downstream transcription factor mediating the function of TAZ. Disruption of TEAD-TAZ binding or silencing of TEAD expression blocked the function of TAZ to promote cell proliferation and to induce epithelial-mesenchymal transition, demonstrating TEAD as a key downstream effector of TAZ. We also identified CTGF, a gene that regulates cell adhesion, proliferation, and migration, as a direct target of TAZ and TEAD. Our study establishes a functional partnership between TAZ and TEAD under negative regulation by the Hippo signaling pathway.

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