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New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis

Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, self-...

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Detalles Bibliográficos
Autores principales: Han, Chang-chang, Wan, Fu-sheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Breast Cancer Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6310719/
https://www.ncbi.nlm.nih.gov/pubmed/30607156
http://dx.doi.org/10.4048/jbc.2018.21.e51
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author Han, Chang-chang
Wan, Fu-sheng
author_facet Han, Chang-chang
Wan, Fu-sheng
author_sort Han, Chang-chang
collection PubMed
description Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, self-protecting signal transduction pathway called the unfolded protein response. Notably, ERS signaling is involved in the development of a variety of diseases and is closely related to tumor development, particularly in breast cancer. This review discusses recent research regarding associations between ERS and tumor metastasis. The information presented here will help researchers elucidate the precise mechanisms underlying ERS-mediated tumor metastasis and provide new directions for tumor therapies.
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spelling pubmed-63107192019-01-03 New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis Han, Chang-chang Wan, Fu-sheng J Breast Cancer Review Article Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, self-protecting signal transduction pathway called the unfolded protein response. Notably, ERS signaling is involved in the development of a variety of diseases and is closely related to tumor development, particularly in breast cancer. This review discusses recent research regarding associations between ERS and tumor metastasis. The information presented here will help researchers elucidate the precise mechanisms underlying ERS-mediated tumor metastasis and provide new directions for tumor therapies. Korean Breast Cancer Society 2018-12 2018-11-23 /pmc/articles/PMC6310719/ /pubmed/30607156 http://dx.doi.org/10.4048/jbc.2018.21.e51 Text en © 2018 Korean Breast Cancer Society http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Han, Chang-chang
Wan, Fu-sheng
New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title_full New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title_fullStr New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title_full_unstemmed New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title_short New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis
title_sort new insights into the role of endoplasmic reticulum stress in breast cancer metastasis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6310719/
https://www.ncbi.nlm.nih.gov/pubmed/30607156
http://dx.doi.org/10.4048/jbc.2018.21.e51
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