Mechanisms of YAP/TAZ transcriptional control

Authors:

Giusy Battilana1, Francesca Zanconato1 and Stefano Piccolo1,2
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Affiliations:

1 Department of Molecular Medicine, University of Padua, Via G. Colombo 3, 35131, Padua, Italy.

2 IFOM, the FIRC Institute of Molecular Oncology, Milan, Italy.

Keywords: 

YAP/TAZ, cancer, Mechanotransduction, Hippo, Brd4, AP-1, proliferation.

Abbreviatons:

CC – coiled-coil,

CRC – colorectal cancer,

ECM – extracellular matrix,

Pol2 – RNA polymerase II.

Corresponding Author(s):

Stefano Piccolo, Department of Molecular Medicine, University of Padua, Via G. Colombo 3, 35131, Padua, Italy; piccolo@bio.unipd.it

Conflict of interest statement:

The authors declare no conflicts of interest.

Please cite this article as:

Giusy Battilana, Francesca Zanconato and Stefano Piccolo (2021). Mechanisms of YAP/TAZ transcriptional control. Cell Stress 5(11): 167-172. doi: 10.15698/cst2021.11.258

© 2021 Battilana et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.

Abstract:

Dysregulated gene expression is intrinsic to cell transformation, tumorigenesis and metastasis. Cancer-specific gene-expression profiles stem from gene regulatory networks fueled by genetic and epigenetic defects, and by abnormal signals of the tumor microenvironment. These oncogenic signals ultimately engage the transcriptional machinery on the cis -regulatory elements of a host of effector genes, through recruitment of transcription factors (TFs), co-activators and chromatin regulators. That said, whether gene -expression in cancer cells is the chaotic product of myriad regulations or rather a relatively ordered process orchestrated by few TFs (master regulators) has long remained enigmatic. Recent work on the YAP/TAZ co-activators has been instrumental to break new ground into this outstanding issue, revealing that tumor cells hijack growth programs that are active during development and regeneration through engagement of a small set of interconnected TFs and their nuclear partners.