TEAD mediates YAP-dependent gene induction and growth control

TEAD mediates YAP-dependent gene induction and growth control

2008 | Bin Zhao, Xin Ye, Jindan Yu, Li Li, Weiqian Li, Siming Li, Jianjun Yu, Jiandie D. Lin, Cun-Yu Wang, Arul M. Chinnaiyan, Zhi-Chun Lai, Kun-Liang Guan
The TEAD family of transcription factors plays a critical role in mediating YAP-dependent gene expression and cell growth. YAP, a transcription coactivator, is involved in oncogenesis and is regulated by the Hippo pathway, which inhibits YAP through phosphorylation. This study demonstrates that TEAD is essential for YAP to induce gene expression, promote cell growth, and drive epithelial-mesenchymal transition (EMT). CTGF, a direct target gene of YAP and TEAD, is crucial for cell growth. The functional relationship between YAP and TEAD is conserved in Drosophila, where Yki (YAP homolog) and Scalloped (TEAD homolog) interact to regulate tissue growth. TEAD is identified as a key component of the Hippo pathway, mediating YAP's biological functions. The study also shows that TEAD is required for YAP-induced growth and oncogenic transformation. Knockdown of TEAD or CTGF significantly reduces YAP-induced cell growth and EMT. These findings highlight TEAD's essential role in YAP signaling and its importance in cancer development.The TEAD family of transcription factors plays a critical role in mediating YAP-dependent gene expression and cell growth. YAP, a transcription coactivator, is involved in oncogenesis and is regulated by the Hippo pathway, which inhibits YAP through phosphorylation. This study demonstrates that TEAD is essential for YAP to induce gene expression, promote cell growth, and drive epithelial-mesenchymal transition (EMT). CTGF, a direct target gene of YAP and TEAD, is crucial for cell growth. The functional relationship between YAP and TEAD is conserved in Drosophila, where Yki (YAP homolog) and Scalloped (TEAD homolog) interact to regulate tissue growth. TEAD is identified as a key component of the Hippo pathway, mediating YAP's biological functions. The study also shows that TEAD is required for YAP-induced growth and oncogenic transformation. Knockdown of TEAD or CTGF significantly reduces YAP-induced cell growth and EMT. These findings highlight TEAD's essential role in YAP signaling and its importance in cancer development.
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