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Roles of Extracellular Vesicles in Metastatic Breast Cancer

Cells can secrete extracellular vesicles (EVs) to communicate with neighboring or distant cells by EVs which are composed of a lipid bilayer containing transmembrane proteins and enclosing cytosolic proteins, lipids, and nucleic acids. Breast Cancer is the most frequently diagnosed malignancy with m...

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Detalles Bibliográficos
Autores principales: Peng, Junya, Wang, Wenqian, Hua, Surong, Liu, Lulu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5987895/
https://www.ncbi.nlm.nih.gov/pubmed/29881285
http://dx.doi.org/10.1177/1178223418767666
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author Peng, Junya
Wang, Wenqian
Hua, Surong
Liu, Lulu
author_facet Peng, Junya
Wang, Wenqian
Hua, Surong
Liu, Lulu
author_sort Peng, Junya
collection PubMed
description Cells can secrete extracellular vesicles (EVs) to communicate with neighboring or distant cells by EVs which are composed of a lipid bilayer containing transmembrane proteins and enclosing cytosolic proteins, lipids, and nucleic acids. Breast Cancer is the most frequently diagnosed malignancy with more than 1 million new cases each year and ranks the leading cause of cancer mortality in women worldwide. In this review, we will discuss recent progresses of the roles and mechanisms of cancer-derived EVs in metastatic breast cancer, with a special attention on tumor microenvironment construction, progression, and chemo/radiotherapy responses. This review also covers EV roles as biomarker and therapeutic target in clinical application.
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spelling pubmed-59878952018-06-07 Roles of Extracellular Vesicles in Metastatic Breast Cancer Peng, Junya Wang, Wenqian Hua, Surong Liu, Lulu Breast Cancer (Auckl) Review: Special Collection: Cell Signaling in Breast Cancer Progression and Metastasis Cells can secrete extracellular vesicles (EVs) to communicate with neighboring or distant cells by EVs which are composed of a lipid bilayer containing transmembrane proteins and enclosing cytosolic proteins, lipids, and nucleic acids. Breast Cancer is the most frequently diagnosed malignancy with more than 1 million new cases each year and ranks the leading cause of cancer mortality in women worldwide. In this review, we will discuss recent progresses of the roles and mechanisms of cancer-derived EVs in metastatic breast cancer, with a special attention on tumor microenvironment construction, progression, and chemo/radiotherapy responses. This review also covers EV roles as biomarker and therapeutic target in clinical application. SAGE Publications 2018-04-25 /pmc/articles/PMC5987895/ /pubmed/29881285 http://dx.doi.org/10.1177/1178223418767666 Text en © The Author(s) 2018 http://www.creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Review: Special Collection: Cell Signaling in Breast Cancer Progression and Metastasis
Peng, Junya
Wang, Wenqian
Hua, Surong
Liu, Lulu
Roles of Extracellular Vesicles in Metastatic Breast Cancer
title Roles of Extracellular Vesicles in Metastatic Breast Cancer
title_full Roles of Extracellular Vesicles in Metastatic Breast Cancer
title_fullStr Roles of Extracellular Vesicles in Metastatic Breast Cancer
title_full_unstemmed Roles of Extracellular Vesicles in Metastatic Breast Cancer
title_short Roles of Extracellular Vesicles in Metastatic Breast Cancer
title_sort roles of extracellular vesicles in metastatic breast cancer
topic Review: Special Collection: Cell Signaling in Breast Cancer Progression and Metastasis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5987895/
https://www.ncbi.nlm.nih.gov/pubmed/29881285
http://dx.doi.org/10.1177/1178223418767666
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