The TEAD Family and Its Oncogenic Role in Promoting Tumorigenesis
AbstractThe TEAD family of transcription factors is necessary for developmental processes. The family members contain a TEA domain for the binding with DNA elements and a transactivation domain for the interaction with transcription coactivators. TEAD proteins are required for the participation of coactivators to transmit the signal of pathways for the downstream signaling processes. TEADs also play an important role in tumor initiation and facilitate cancer progression via activating a series of progression-inducing genes, such as CTGF, Cyr61, Myc and Gli2. Recent studies have highlighted that TEADs, together with their coactivators, promote or even act as the crucial parts in the development of various malignancies, such as liver, ovarian, breast and prostate cancers. Furthermore, TEADs are proposed to be useful prognostic biomarkers due to the ideal correlation between high expression and clinicopathological parameters in gastric, breast, ovarian and prostate cancers. In this review, we summarize the functional role of TEAD proteins in tumorigenesis and discuss the key role of TEAD transcription factors in the linking of signal cascade transductions. Improved knowledge of the TEAD proteins will be helpful for deep understanding of the molecular mechanisms of tumorigenesis and identifying ideal predictive or prognostic biomarkers, even providing clinical translation for anticancer therapy in human cancers. View Full-Text
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Zhou, Y.; Huang, T.; Cheng, A.S.L.; Yu, J.; Kang, W.; To, K.F. The TEAD Family and Its Oncogenic Role in Promoting Tumorigenesis. Int. J. Mol. Sci. 2016, 17, 138.
Zhou Y, Huang T, Cheng ASL, Yu J, Kang W, To KF. The TEAD Family and Its Oncogenic Role in Promoting Tumorigenesis. International Journal of Molecular Sciences. 2016; 17(1):138.Chicago/Turabian Style
Zhou, Yuhang; Huang, Tingting; Cheng, Alfred S.L.; Yu, Jun; Kang, Wei; To, Ka F. 2016. "The TEAD Family and Its Oncogenic Role in Promoting Tumorigenesis." Int. J. Mol. Sci. 17, no. 1: 138.
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