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Mechanisms of YAP/TAZ transcriptional control

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 ultimat...

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Detalles Bibliográficos
Autores principales: Battilana, Giusy, Zanconato, Francesca, Piccolo, Stefano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shared Science Publishers OG 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8561301/
https://www.ncbi.nlm.nih.gov/pubmed/34782888
http://dx.doi.org/10.15698/cst2021.11.258
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author Battilana, Giusy
Zanconato, Francesca
Piccolo, Stefano
author_facet Battilana, Giusy
Zanconato, Francesca
Piccolo, Stefano
author_sort Battilana, Giusy
collection PubMed
description 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.
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spelling pubmed-85613012021-11-14 Mechanisms of YAP/TAZ transcriptional control Battilana, Giusy Zanconato, Francesca Piccolo, Stefano Cell Stress Review 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. Shared Science Publishers OG 2021-10-29 /pmc/articles/PMC8561301/ /pubmed/34782888 http://dx.doi.org/10.15698/cst2021.11.258 Text en Copyright: © 2021 Battilana et al. https://creativecommons.org/licenses/by/4.0/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 reproduction in any medium, provided the original author and source are acknowledged.
spellingShingle Review
Battilana, Giusy
Zanconato, Francesca
Piccolo, Stefano
Mechanisms of YAP/TAZ transcriptional control
title Mechanisms of YAP/TAZ transcriptional control
title_full Mechanisms of YAP/TAZ transcriptional control
title_fullStr Mechanisms of YAP/TAZ transcriptional control
title_full_unstemmed Mechanisms of YAP/TAZ transcriptional control
title_short Mechanisms of YAP/TAZ transcriptional control
title_sort mechanisms of yap/taz transcriptional control
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8561301/
https://www.ncbi.nlm.nih.gov/pubmed/34782888
http://dx.doi.org/10.15698/cst2021.11.258
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