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Roles of ARID1A variations in colorectal cancer: a collaborative review

Colorectal cancer (CRC), a common malignancy, is one of the leading cause of cancer death in adults. AT-rich interaction domain 1A (ARID1A), a critical portion of the SWItch/sucrose non-fermentation (SWI/SNF) chromatin remodeling complexes, shows one of the most frequent mutant genes across differen...

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Autores principales: Zhao, Shankun, Wu, Weizhou, Jiang, Zufu, Tang, Fuqin, Ding, Lingzhi, Xu, Weifang, Ruan, Libin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009033/
https://www.ncbi.nlm.nih.gov/pubmed/35421925
http://dx.doi.org/10.1186/s10020-022-00469-6
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author Zhao, Shankun
Wu, Weizhou
Jiang, Zufu
Tang, Fuqin
Ding, Lingzhi
Xu, Weifang
Ruan, Libin
author_facet Zhao, Shankun
Wu, Weizhou
Jiang, Zufu
Tang, Fuqin
Ding, Lingzhi
Xu, Weifang
Ruan, Libin
author_sort Zhao, Shankun
collection PubMed
description Colorectal cancer (CRC), a common malignancy, is one of the leading cause of cancer death in adults. AT-rich interaction domain 1A (ARID1A), a critical portion of the SWItch/sucrose non-fermentation (SWI/SNF) chromatin remodeling complexes, shows one of the most frequent mutant genes across different human cancer types. Deleterious variations of ARID1A has been recognized to be correlated the tumorigenesis and the poor prognosis of CRC. Here, we summarize recent advances in the clinical implications and molecular pathogenesis of ARID1A variations in CRC. According to independent data of 23 included studies, ARID1A is mutated in 3.6–66.7%. Consistently, all of the 23 relevant studies report that ARID1A functions as a specific tumor suppressor in CRC. Clinically, ARID1A variation status serves as a biomarker for survival prognosis and various therapies for CRC. Mechanistically, the pathophysiologic impacts of ARID1A variations on CRC may be associated with the co-occurrence variations of other genes (i.e., TP53, KRAS, APC, FBXW7, and PIK3CA) and the regulation of several signaling pathways being affected (i.e., WNT signaling, Akt signaling, and MEK/ERK pathway), leading to cell cycle arrest, chromatin remodeling, chromosome organization, and DNA hypermethylation of the cancer cells. The present review highlights ARID1A serving as a potent tumor suppressor and an important prognostic factor in CRC. ARID1A variations hint towards a promising tool for diagnostic tumor profiling and individualized therapeutic targets for CRC in the future.
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spelling pubmed-90090332022-04-15 Roles of ARID1A variations in colorectal cancer: a collaborative review Zhao, Shankun Wu, Weizhou Jiang, Zufu Tang, Fuqin Ding, Lingzhi Xu, Weifang Ruan, Libin Mol Med Review Colorectal cancer (CRC), a common malignancy, is one of the leading cause of cancer death in adults. AT-rich interaction domain 1A (ARID1A), a critical portion of the SWItch/sucrose non-fermentation (SWI/SNF) chromatin remodeling complexes, shows one of the most frequent mutant genes across different human cancer types. Deleterious variations of ARID1A has been recognized to be correlated the tumorigenesis and the poor prognosis of CRC. Here, we summarize recent advances in the clinical implications and molecular pathogenesis of ARID1A variations in CRC. According to independent data of 23 included studies, ARID1A is mutated in 3.6–66.7%. Consistently, all of the 23 relevant studies report that ARID1A functions as a specific tumor suppressor in CRC. Clinically, ARID1A variation status serves as a biomarker for survival prognosis and various therapies for CRC. Mechanistically, the pathophysiologic impacts of ARID1A variations on CRC may be associated with the co-occurrence variations of other genes (i.e., TP53, KRAS, APC, FBXW7, and PIK3CA) and the regulation of several signaling pathways being affected (i.e., WNT signaling, Akt signaling, and MEK/ERK pathway), leading to cell cycle arrest, chromatin remodeling, chromosome organization, and DNA hypermethylation of the cancer cells. The present review highlights ARID1A serving as a potent tumor suppressor and an important prognostic factor in CRC. ARID1A variations hint towards a promising tool for diagnostic tumor profiling and individualized therapeutic targets for CRC in the future. BioMed Central 2022-04-14 /pmc/articles/PMC9009033/ /pubmed/35421925 http://dx.doi.org/10.1186/s10020-022-00469-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
Zhao, Shankun
Wu, Weizhou
Jiang, Zufu
Tang, Fuqin
Ding, Lingzhi
Xu, Weifang
Ruan, Libin
Roles of ARID1A variations in colorectal cancer: a collaborative review
title Roles of ARID1A variations in colorectal cancer: a collaborative review
title_full Roles of ARID1A variations in colorectal cancer: a collaborative review
title_fullStr Roles of ARID1A variations in colorectal cancer: a collaborative review
title_full_unstemmed Roles of ARID1A variations in colorectal cancer: a collaborative review
title_short Roles of ARID1A variations in colorectal cancer: a collaborative review
title_sort roles of arid1a variations in colorectal cancer: a collaborative review
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009033/
https://www.ncbi.nlm.nih.gov/pubmed/35421925
http://dx.doi.org/10.1186/s10020-022-00469-6
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