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Biochem. Biophys. Res. Commun. · Apr 2017
TEAD4-YAP interaction regulates tumoral growth by controlling cell-cycle arrest at the G1 phase.
- Shin Takeuchi, Atsushi Kasamatsu, Masanobu Yamatoji, Dai Nakashima, Yosuke Endo-Sakamoto, Nao Koide, Toshikazu Takahara, Toshihiro Shimizu, Manabu Iyoda, Katsunori Ogawara, Masashi Shiiba, Hideki Tanzawa, and Katsuhiro Uzawa.
- Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba, Japan.
- Biochem. Biophys. Res. Commun. 2017 Apr 29; 486 (2): 385-390.
AbstractTEA domain transcription factor 4 (TEAD4), which has critical functions in the process of embryonic development, is expressed in various cancers. However, the important role of TEAD4 in human oral squamous cell carcinomas (OSCCs) remain unclear. Here we investigated the TEAD4 expression level and the functional mechanism in OSCC using quantitative reverse transcriptase-polymerase chain reaction, Western blot analysis, and immunohistochemistry. Furthermore, TEAD4 knockdown model was used to evaluate cellular proliferation, cell-cycle analysis, and the interaction between TEAD4 and Yes-associated protein (YAP) which was reported to be a transcription coactivator of cellular proliferation. In the current study, we found that TEAD4 expression increased significantly in vitro and in vivo and correlated with tumoral size in OSCC patients. TEAD4 knockdown OSCC cells showed decreased cellular proliferation resulting from cell-cycle arrest in the G1 phase by down-regulation of cyclins, cyclin-dependent kinases (CDKs), and up-regulation of CDK inhibitors. We also found that the TEAD4-YAP complex in the nuclei may be related closely to transcriptions of G1 arrest-related genes. Taken together, we concluded that TEAD4 might play an important role in tumoral growth and have potential to be a therapeutic target in OSCCs.Copyright © 2017 Elsevier Inc. All rights reserved.
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