Next Article in Journal
TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease
Previous Article in Journal
RK-33 Is a Broad-Spectrum Antiviral Agent That Targets DEAD-Box RNA Helicase DDX3X
Open AccessArticle

Transcriptional Coactivator TAZ Negatively Regulates Tumor Suppressor p53 Activity and Cellular Senescence

1
Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan
2
Department of Innovative Therapeutic Sciences, Cooperative Major in Nanopharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan
3
Division of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kanagawa 210-9501, Japan
4
Department of Molecular Medicine for Pathogenesis, Graduate School of Medicine, Ehime University, Ehime 791-0295, Japan
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2020, 9(1), 171; https://doi.org/10.3390/cells9010171
Received: 7 November 2019 / Revised: 31 December 2019 / Accepted: 8 January 2020 / Published: 9 January 2020
(This article belongs to the Special Issue Role of p53 in Cell Death and Cancers)
Transcriptional coactivator with a PDZ-binding motif (TAZ) is one of the mammalian orthologs of Drosophila Yorkie, a transcriptional coactivator of the Hippo pathway. TAZ has been suggested to function as a regulator that modulates the expression of cell proliferation and anti-apoptotic genes in order to stimulate cell proliferation. TAZ has also been associated with a poor prognosis in several cancers, including breast cancer. However, the physiological role of TAZ in tumorigenesis remains unclear. We herein demonstrated that TAZ negatively regulated the activity of the tumor suppressor p53. The overexpression of TAZ down-regulated p53 transcriptional activity and its downstream gene expression. In contrast, TAZ knockdown up-regulated p21 expression induced by p53 activation. Regarding the underlying mechanism, TAZ inhibited the interaction between p53 and p300 and suppressed the p300-mediated acetylation of p53. Furthermore, TAZ knockdown induced cellular senescence in a p53-dependent manner. These results suggest that TAZ negatively regulates the tumor suppressor functions of p53 and attenuates p53-mediated cellular senescence.
Keywords: cellular senescence; oncogene; p300; p53; TAZ cellular senescence; oncogene; p300; p53; TAZ
MDPI and ACS Style

Miyajima, C.; Kawarada, Y.; Inoue, Y.; Suzuki, C.; Mitamura, K.; Morishita, D.; Ohoka, N.; Imamura, T.; Hayashi, H. Transcriptional Coactivator TAZ Negatively Regulates Tumor Suppressor p53 Activity and Cellular Senescence. Cells 2020, 9, 171.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop