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To bind or not to bind: Cistromic reprogramming in prostate cancer
The term “cistrome” refers to the genome-wide location of regulatory elements associated with transcription factor binding-sites. The cistrome of key regulatory factors in prostate cancer etiology are substantially reprogrammed and altered during prostatic transformation and disease progression. For...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539323/ https://www.ncbi.nlm.nih.gov/pubmed/36212399 http://dx.doi.org/10.3389/fonc.2022.963007 |
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author | Shen, Michelle Demers, Léa-Kristine Bailey, Swneke D. Labbé, David P. |
author_facet | Shen, Michelle Demers, Léa-Kristine Bailey, Swneke D. Labbé, David P. |
author_sort | Shen, Michelle |
collection | PubMed |
description | The term “cistrome” refers to the genome-wide location of regulatory elements associated with transcription factor binding-sites. The cistrome of key regulatory factors in prostate cancer etiology are substantially reprogrammed and altered during prostatic transformation and disease progression. For instance, the cistrome of the androgen receptor (AR), a ligand-inducible transcription factor central in normal prostate epithelium biology, is directly impacted and substantially reprogrammed during malignant transformation. Accumulating evidence demonstrates that additional transcription factors that are frequently mutated, or aberrantly expressed in prostate cancer, such as the pioneer transcription factors Forkhead Box A1 (FOXA1), the homeobox protein HOXB13, and the GATA binding protein 2 (GATA2), and the ETS-related gene (ERG), and the MYC proto-oncogene, contribute to the reprogramming of the AR cistrome. In addition, recent findings have highlighted key roles for the SWI/SNF complex and the chromatin-modifying helicase CHD1 in remodeling the epigenome and altering the AR cistrome during disease progression. In this review, we will cover the role of cistromic reprogramming in prostate cancer initiation and progression. Specifically, we will discuss the impact of key prostate cancer regulators, as well as the role of epigenetic and chromatin regulators in relation to the AR cistrome and the transformation of normal prostate epithelium. Given the importance of chromatin-transcription factor dynamics in normal cellular differentiation and cancer, an in-depth assessment of the factors involved in producing these altered cistromes is of great relevance and provides insight into new therapeutic strategies for prostate cancer. |
format | Online Article Text |
id | pubmed-9539323 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95393232022-10-08 To bind or not to bind: Cistromic reprogramming in prostate cancer Shen, Michelle Demers, Léa-Kristine Bailey, Swneke D. Labbé, David P. Front Oncol Oncology The term “cistrome” refers to the genome-wide location of regulatory elements associated with transcription factor binding-sites. The cistrome of key regulatory factors in prostate cancer etiology are substantially reprogrammed and altered during prostatic transformation and disease progression. For instance, the cistrome of the androgen receptor (AR), a ligand-inducible transcription factor central in normal prostate epithelium biology, is directly impacted and substantially reprogrammed during malignant transformation. Accumulating evidence demonstrates that additional transcription factors that are frequently mutated, or aberrantly expressed in prostate cancer, such as the pioneer transcription factors Forkhead Box A1 (FOXA1), the homeobox protein HOXB13, and the GATA binding protein 2 (GATA2), and the ETS-related gene (ERG), and the MYC proto-oncogene, contribute to the reprogramming of the AR cistrome. In addition, recent findings have highlighted key roles for the SWI/SNF complex and the chromatin-modifying helicase CHD1 in remodeling the epigenome and altering the AR cistrome during disease progression. In this review, we will cover the role of cistromic reprogramming in prostate cancer initiation and progression. Specifically, we will discuss the impact of key prostate cancer regulators, as well as the role of epigenetic and chromatin regulators in relation to the AR cistrome and the transformation of normal prostate epithelium. Given the importance of chromatin-transcription factor dynamics in normal cellular differentiation and cancer, an in-depth assessment of the factors involved in producing these altered cistromes is of great relevance and provides insight into new therapeutic strategies for prostate cancer. Frontiers Media S.A. 2022-09-23 /pmc/articles/PMC9539323/ /pubmed/36212399 http://dx.doi.org/10.3389/fonc.2022.963007 Text en Copyright © 2022 Shen, Demers, Bailey and Labbé https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Oncology Shen, Michelle Demers, Léa-Kristine Bailey, Swneke D. Labbé, David P. To bind or not to bind: Cistromic reprogramming in prostate cancer |
title | To bind or not to bind: Cistromic reprogramming in prostate cancer |
title_full | To bind or not to bind: Cistromic reprogramming in prostate cancer |
title_fullStr | To bind or not to bind: Cistromic reprogramming in prostate cancer |
title_full_unstemmed | To bind or not to bind: Cistromic reprogramming in prostate cancer |
title_short | To bind or not to bind: Cistromic reprogramming in prostate cancer |
title_sort | to bind or not to bind: cistromic reprogramming in prostate cancer |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9539323/ https://www.ncbi.nlm.nih.gov/pubmed/36212399 http://dx.doi.org/10.3389/fonc.2022.963007 |
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