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Endoplasmic reticulum stress targeted therapy for breast cancer
Recurrence, metastasis, and drug resistance are still big challenges in breast cancer therapy. Internal and external stresses have been proven to substantially facilitate breast cancer progression through molecular and systemic mechanisms. For example, endoplasmic reticulum stress (ERS) results in a...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9639265/ https://www.ncbi.nlm.nih.gov/pubmed/36345017 http://dx.doi.org/10.1186/s12964-022-00964-7 |
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author | Xu, Di Liu, Zhen Liang, Ming-Xing Fei, Yin-Jiao Zhang, Wei Wu, Yang Tang, Jin-Hai |
author_facet | Xu, Di Liu, Zhen Liang, Ming-Xing Fei, Yin-Jiao Zhang, Wei Wu, Yang Tang, Jin-Hai |
author_sort | Xu, Di |
collection | PubMed |
description | Recurrence, metastasis, and drug resistance are still big challenges in breast cancer therapy. Internal and external stresses have been proven to substantially facilitate breast cancer progression through molecular and systemic mechanisms. For example, endoplasmic reticulum stress (ERS) results in activation of the unfolded protein response (UPR), which are considered an important cellular stress response. More and more reports indicate its key role in protein homeostasis and other diverse functions involved in the process of breast cancer progression. Therefore, therapies targeting the activation of ERS and its downstream signaling pathways are potentially helpful and novel tools to counteract and fight breast cancer. However, recent advances in our understanding of ERS are focused on characterizing and modulating ERS between healthy and disease states, and so little attention has been paid to studying the role and clinical application of targeting ERS in a certain cancer. In this review, we summarize the function and main mechanisms of ERS in different molecular types of breast cancer, and focus on the development of agents targeting ERS to provide new treatment strategies for breast cancer. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-022-00964-7. |
format | Online Article Text |
id | pubmed-9639265 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-96392652022-11-08 Endoplasmic reticulum stress targeted therapy for breast cancer Xu, Di Liu, Zhen Liang, Ming-Xing Fei, Yin-Jiao Zhang, Wei Wu, Yang Tang, Jin-Hai Cell Commun Signal Review Recurrence, metastasis, and drug resistance are still big challenges in breast cancer therapy. Internal and external stresses have been proven to substantially facilitate breast cancer progression through molecular and systemic mechanisms. For example, endoplasmic reticulum stress (ERS) results in activation of the unfolded protein response (UPR), which are considered an important cellular stress response. More and more reports indicate its key role in protein homeostasis and other diverse functions involved in the process of breast cancer progression. Therefore, therapies targeting the activation of ERS and its downstream signaling pathways are potentially helpful and novel tools to counteract and fight breast cancer. However, recent advances in our understanding of ERS are focused on characterizing and modulating ERS between healthy and disease states, and so little attention has been paid to studying the role and clinical application of targeting ERS in a certain cancer. In this review, we summarize the function and main mechanisms of ERS in different molecular types of breast cancer, and focus on the development of agents targeting ERS to provide new treatment strategies for breast cancer. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-022-00964-7. BioMed Central 2022-11-07 /pmc/articles/PMC9639265/ /pubmed/36345017 http://dx.doi.org/10.1186/s12964-022-00964-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Xu, Di Liu, Zhen Liang, Ming-Xing Fei, Yin-Jiao Zhang, Wei Wu, Yang Tang, Jin-Hai Endoplasmic reticulum stress targeted therapy for breast cancer |
title | Endoplasmic reticulum stress targeted therapy for breast cancer |
title_full | Endoplasmic reticulum stress targeted therapy for breast cancer |
title_fullStr | Endoplasmic reticulum stress targeted therapy for breast cancer |
title_full_unstemmed | Endoplasmic reticulum stress targeted therapy for breast cancer |
title_short | Endoplasmic reticulum stress targeted therapy for breast cancer |
title_sort | endoplasmic reticulum stress targeted therapy for breast cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9639265/ https://www.ncbi.nlm.nih.gov/pubmed/36345017 http://dx.doi.org/10.1186/s12964-022-00964-7 |
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