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Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers
The unfolded protein response (UPR) is an ancient stress response that enables a cell to manage the energetic stress that accompanies protein folding. There has been a significant recent increase in our understanding of the UPR, how it integrates physiological processes within cells, and how this in...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4475795/ https://www.ncbi.nlm.nih.gov/pubmed/26157705 http://dx.doi.org/10.3389/fonc.2015.00140 |
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author | Clarke, Robert Cook, Katherine L. |
author_facet | Clarke, Robert Cook, Katherine L. |
author_sort | Clarke, Robert |
collection | PubMed |
description | The unfolded protein response (UPR) is an ancient stress response that enables a cell to manage the energetic stress that accompanies protein folding. There has been a significant recent increase in our understanding of the UPR, how it integrates physiological processes within cells, and how this integration can affect cancer cells and cell fate decisions. Recent publications have highlighted the role of UPR signaling components on mediating various cell survival pathways, cellular metabolism and bioenergenics, and autophagy. We address the role of UPR on mediating endocrine therapy resistance and estrogen receptor-positive breast cancer cell survival. |
format | Online Article Text |
id | pubmed-4475795 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-44757952015-07-08 Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers Clarke, Robert Cook, Katherine L. Front Oncol Oncology The unfolded protein response (UPR) is an ancient stress response that enables a cell to manage the energetic stress that accompanies protein folding. There has been a significant recent increase in our understanding of the UPR, how it integrates physiological processes within cells, and how this integration can affect cancer cells and cell fate decisions. Recent publications have highlighted the role of UPR signaling components on mediating various cell survival pathways, cellular metabolism and bioenergenics, and autophagy. We address the role of UPR on mediating endocrine therapy resistance and estrogen receptor-positive breast cancer cell survival. Frontiers Media S.A. 2015-06-22 /pmc/articles/PMC4475795/ /pubmed/26157705 http://dx.doi.org/10.3389/fonc.2015.00140 Text en Copyright © 2015 Clarke and Cook. 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 Clarke, Robert Cook, Katherine L. Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title | Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title_full | Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title_fullStr | Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title_full_unstemmed | Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title_short | Unfolding the Role of Stress Response Signaling in Endocrine Resistant Breast Cancers |
title_sort | unfolding the role of stress response signaling in endocrine resistant breast cancers |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4475795/ https://www.ncbi.nlm.nih.gov/pubmed/26157705 http://dx.doi.org/10.3389/fonc.2015.00140 |
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