title: TEAD transcription factors mediate the function of TAZ in cell growth and epithelial-mesenchymal transition.
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.
authors.affiliation: Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; School of Life Science Fudan University, Shanghai, China 200032.
authors.forename: Heng
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; School of Life Science Fudan University, Shanghai, China 200032.
authors.forename: Chen-Ying
authors.initials: CY
authors.lastname: Liu
authors.affiliation: Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032.
authors.forename: Zheng-Yu
authors.initials: ZY
authors.lastname: Zha
authors.affiliation: Department of Pharmacology and Moores Cancer Center, University of California at San Diego, La Jolla, California 92093-0815.
authors.forename: Bin
authors.initials: B
authors.lastname: Zhao
authors.affiliation: Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032.
authors.forename: Jun
authors.initials: J
authors.lastname: Yao
authors.affiliation: Molecular and Cell Biology Laboratory, Institutes of Biomedical Sciences Fudan University, Shanghai, China 200032; School of Life Science Fudan University, Shanghai, China 200032.
authors.forename: Shimin
authors.initials: S
authors.lastname: Zhao
authors.affiliation: 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.
authors.forename: Yue
authors.initials: Y
authors.lastname: Xiong
authors.affiliation: 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.
authors.forename: Qun-Ying
authors.initials: QY
authors.lastname: Lei
authors.affiliation: 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.
authors.forename: Kun-Liang
authors.initials: KL
authors.lastname: Guan