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Restructuring of Lamina-Associated Domains in Senescence and Cancer
Induction of cellular senescence or cancer is associated with a reshaping of the nuclear envelope and a broad reorganization of heterochromatin. At the periphery of mammalian nuclei, heterochromatin is stabilized at the nuclear lamina via lamina-associated domains (LADs). Alterations in the composit...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9180887/ https://www.ncbi.nlm.nih.gov/pubmed/35681541 http://dx.doi.org/10.3390/cells11111846 |
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author | Bellanger, Aurélie Madsen-Østerbye, Julia Galigniana, Natalia M. Collas, Philippe |
author_facet | Bellanger, Aurélie Madsen-Østerbye, Julia Galigniana, Natalia M. Collas, Philippe |
author_sort | Bellanger, Aurélie |
collection | PubMed |
description | Induction of cellular senescence or cancer is associated with a reshaping of the nuclear envelope and a broad reorganization of heterochromatin. At the periphery of mammalian nuclei, heterochromatin is stabilized at the nuclear lamina via lamina-associated domains (LADs). Alterations in the composition of the nuclear lamina during senescence lead to a loss of peripheral heterochromatin, repositioning of LADs, and changes in epigenetic states of LADs. Cancer initiation and progression are also accompanied by a massive reprogramming of the epigenome, particularly in domains coinciding with LADs. Here, we review recent knowledge on alterations in chromatin organization and in the epigenome that affect LADs and related genomic domains in senescence and cancer. |
format | Online Article Text |
id | pubmed-9180887 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-91808872022-06-10 Restructuring of Lamina-Associated Domains in Senescence and Cancer Bellanger, Aurélie Madsen-Østerbye, Julia Galigniana, Natalia M. Collas, Philippe Cells Review Induction of cellular senescence or cancer is associated with a reshaping of the nuclear envelope and a broad reorganization of heterochromatin. At the periphery of mammalian nuclei, heterochromatin is stabilized at the nuclear lamina via lamina-associated domains (LADs). Alterations in the composition of the nuclear lamina during senescence lead to a loss of peripheral heterochromatin, repositioning of LADs, and changes in epigenetic states of LADs. Cancer initiation and progression are also accompanied by a massive reprogramming of the epigenome, particularly in domains coinciding with LADs. Here, we review recent knowledge on alterations in chromatin organization and in the epigenome that affect LADs and related genomic domains in senescence and cancer. MDPI 2022-06-05 /pmc/articles/PMC9180887/ /pubmed/35681541 http://dx.doi.org/10.3390/cells11111846 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Bellanger, Aurélie Madsen-Østerbye, Julia Galigniana, Natalia M. Collas, Philippe Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title | Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title_full | Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title_fullStr | Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title_full_unstemmed | Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title_short | Restructuring of Lamina-Associated Domains in Senescence and Cancer |
title_sort | restructuring of lamina-associated domains in senescence and cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9180887/ https://www.ncbi.nlm.nih.gov/pubmed/35681541 http://dx.doi.org/10.3390/cells11111846 |
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