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Endoplasmic Reticulum Stress, Genome Damage, and Cancer
Endoplasmic reticulum (ER) stress has been linked to many diseases, including cancer. A large body of work has focused on the activation of the ER stress response in cancer cells to facilitate their survival and tumor growth; however, there are some studies suggesting that the ER stress response can...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315039/ https://www.ncbi.nlm.nih.gov/pubmed/25692096 http://dx.doi.org/10.3389/fonc.2015.00011 |
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author | Dicks, Naomi Gutierrez, Karina Michalak, Marek Bordignon, Vilceu Agellon, Luis B. |
author_facet | Dicks, Naomi Gutierrez, Karina Michalak, Marek Bordignon, Vilceu Agellon, Luis B. |
author_sort | Dicks, Naomi |
collection | PubMed |
description | Endoplasmic reticulum (ER) stress has been linked to many diseases, including cancer. A large body of work has focused on the activation of the ER stress response in cancer cells to facilitate their survival and tumor growth; however, there are some studies suggesting that the ER stress response can also mitigate cancer progression. Despite these contradictions, it is clear that the ER stress response is closely associated with cancer biology. The ER stress response classically encompasses activation of three separate pathways, which are collectively categorized the unfolded protein response (UPR). The UPR has been extensively studied in various cancers and appears to confer a selective advantage to tumor cells to facilitate their enhanced growth and resistance to anti-cancer agents. It has also been shown that ER stress induces chromatin changes, which can also facilitate cell survival. Chromatin remodeling has been linked with many cancers through repression of tumor suppressor and apoptosis genes. Interplay between the classic UPR and genome damage repair mechanisms may have important implications in the transformation process of normal cells into cancer cells. |
format | Online Article Text |
id | pubmed-4315039 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-43150392015-02-17 Endoplasmic Reticulum Stress, Genome Damage, and Cancer Dicks, Naomi Gutierrez, Karina Michalak, Marek Bordignon, Vilceu Agellon, Luis B. Front Oncol Oncology Endoplasmic reticulum (ER) stress has been linked to many diseases, including cancer. A large body of work has focused on the activation of the ER stress response in cancer cells to facilitate their survival and tumor growth; however, there are some studies suggesting that the ER stress response can also mitigate cancer progression. Despite these contradictions, it is clear that the ER stress response is closely associated with cancer biology. The ER stress response classically encompasses activation of three separate pathways, which are collectively categorized the unfolded protein response (UPR). The UPR has been extensively studied in various cancers and appears to confer a selective advantage to tumor cells to facilitate their enhanced growth and resistance to anti-cancer agents. It has also been shown that ER stress induces chromatin changes, which can also facilitate cell survival. Chromatin remodeling has been linked with many cancers through repression of tumor suppressor and apoptosis genes. Interplay between the classic UPR and genome damage repair mechanisms may have important implications in the transformation process of normal cells into cancer cells. Frontiers Media S.A. 2015-02-03 /pmc/articles/PMC4315039/ /pubmed/25692096 http://dx.doi.org/10.3389/fonc.2015.00011 Text en Copyright © 2015 Dicks, Gutierrez, Michalak, Bordignon and Agellon. http://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) or licensor 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 Dicks, Naomi Gutierrez, Karina Michalak, Marek Bordignon, Vilceu Agellon, Luis B. Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title | Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title_full | Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title_fullStr | Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title_full_unstemmed | Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title_short | Endoplasmic Reticulum Stress, Genome Damage, and Cancer |
title_sort | endoplasmic reticulum stress, genome damage, and cancer |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315039/ https://www.ncbi.nlm.nih.gov/pubmed/25692096 http://dx.doi.org/10.3389/fonc.2015.00011 |
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