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Endoplasmic Reticulum Stress and Cancer

The endoplasmic reticulum (ER) is the principal organelle responsible for multiple cellular functions including protein folding and maturation and the maintenance of cellular homeostasis. ER stress is activated by a variety of factors and triggers the unfolded protein response (UPR), which restores...

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Autores principales: Yadav, Raj Kumar, Chae, Soo-Wan, Kim, Hyung-Ryong, Chae, Han Jung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society of Cancer Prevention 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204165/
https://www.ncbi.nlm.nih.gov/pubmed/25337575
http://dx.doi.org/10.15430/JCP.2014.19.2.75
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author Yadav, Raj Kumar
Chae, Soo-Wan
Kim, Hyung-Ryong
Chae, Han Jung
author_facet Yadav, Raj Kumar
Chae, Soo-Wan
Kim, Hyung-Ryong
Chae, Han Jung
author_sort Yadav, Raj Kumar
collection PubMed
description The endoplasmic reticulum (ER) is the principal organelle responsible for multiple cellular functions including protein folding and maturation and the maintenance of cellular homeostasis. ER stress is activated by a variety of factors and triggers the unfolded protein response (UPR), which restores homeostasis or activates cell death. Multiple studies have clarified the link between ER stress and cancer, and particularly the involvement of the UPR. The UPR seems to adjust the paradoxical microenvironment of cancer and, as such, is one of resistance mechanisms against cancer therapy. This review describes the activity of different UPRs involved in tumorigenesis and resistance to cancer therapy.
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spelling pubmed-42041652014-10-21 Endoplasmic Reticulum Stress and Cancer Yadav, Raj Kumar Chae, Soo-Wan Kim, Hyung-Ryong Chae, Han Jung J Cancer Prev Review The endoplasmic reticulum (ER) is the principal organelle responsible for multiple cellular functions including protein folding and maturation and the maintenance of cellular homeostasis. ER stress is activated by a variety of factors and triggers the unfolded protein response (UPR), which restores homeostasis or activates cell death. Multiple studies have clarified the link between ER stress and cancer, and particularly the involvement of the UPR. The UPR seems to adjust the paradoxical microenvironment of cancer and, as such, is one of resistance mechanisms against cancer therapy. This review describes the activity of different UPRs involved in tumorigenesis and resistance to cancer therapy. Korean Society of Cancer Prevention 2014-06 /pmc/articles/PMC4204165/ /pubmed/25337575 http://dx.doi.org/10.15430/JCP.2014.19.2.75 Text en Copyright © 2014 Korean Society of Cancer Prevention This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Yadav, Raj Kumar
Chae, Soo-Wan
Kim, Hyung-Ryong
Chae, Han Jung
Endoplasmic Reticulum Stress and Cancer
title Endoplasmic Reticulum Stress and Cancer
title_full Endoplasmic Reticulum Stress and Cancer
title_fullStr Endoplasmic Reticulum Stress and Cancer
title_full_unstemmed Endoplasmic Reticulum Stress and Cancer
title_short Endoplasmic Reticulum Stress and Cancer
title_sort endoplasmic reticulum stress and cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204165/
https://www.ncbi.nlm.nih.gov/pubmed/25337575
http://dx.doi.org/10.15430/JCP.2014.19.2.75
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