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Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications

Epigenetic regulation refers to alterations to the chromatin template that collectively establish differential patterns of gene transcription. Post-translational modifications of the histones play a key role in epigenetic regulation of gene transcription. In this review, we provide an overview of re...

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Autores principales: Zhang, Bao-Jie, Chen, Deng, Dekker, Frank J., Quax, Wim J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: OAE Publishing Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992553/
https://www.ncbi.nlm.nih.gov/pubmed/35582230
http://dx.doi.org/10.20517/cdr.2020.58
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author Zhang, Bao-Jie
Chen, Deng
Dekker, Frank J.
Quax, Wim J.
author_facet Zhang, Bao-Jie
Chen, Deng
Dekker, Frank J.
Quax, Wim J.
author_sort Zhang, Bao-Jie
collection PubMed
description Epigenetic regulation refers to alterations to the chromatin template that collectively establish differential patterns of gene transcription. Post-translational modifications of the histones play a key role in epigenetic regulation of gene transcription. In this review, we provide an overview of recent studies on the role of histone modifications in carcinogenesis. Since tumour-selective ligands such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are well-considered as promising anti-tumour therapies, we summarise strategies for improving TRAIL sensitivity by inhibiting aberrant histone modifications in cancers. In this perspective we also discuss new epigenetic drug targets for enhancing TRAIL-mediated apoptosis.
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spelling pubmed-89925532022-05-16 Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications Zhang, Bao-Jie Chen, Deng Dekker, Frank J. Quax, Wim J. Cancer Drug Resist Review Epigenetic regulation refers to alterations to the chromatin template that collectively establish differential patterns of gene transcription. Post-translational modifications of the histones play a key role in epigenetic regulation of gene transcription. In this review, we provide an overview of recent studies on the role of histone modifications in carcinogenesis. Since tumour-selective ligands such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are well-considered as promising anti-tumour therapies, we summarise strategies for improving TRAIL sensitivity by inhibiting aberrant histone modifications in cancers. In this perspective we also discuss new epigenetic drug targets for enhancing TRAIL-mediated apoptosis. OAE Publishing Inc. 2020-10-09 /pmc/articles/PMC8992553/ /pubmed/35582230 http://dx.doi.org/10.20517/cdr.2020.58 Text en © The Author(s) 2020. https://creativecommons.org/licenses/by/4.0/© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Zhang, Bao-Jie
Chen, Deng
Dekker, Frank J.
Quax, Wim J.
Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title_full Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title_fullStr Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title_full_unstemmed Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title_short Improving TRAIL-induced apoptosis in cancers by interfering with histone modifications
title_sort improving trail-induced apoptosis in cancers by interfering with histone modifications
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992553/
https://www.ncbi.nlm.nih.gov/pubmed/35582230
http://dx.doi.org/10.20517/cdr.2020.58
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