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The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response

Over the past few decades, connexin hemichannels have become recognized as major players in modulating the inflammatory response. Chronic inflammation is documented to promote tumorigenesis and is a critical component of tumor progression. Furthermore, inflammation is strongly linked to angiogenesis...

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Detalles Bibliográficos
Autores principales: Rhett, J. Matthew, Yeh, Elizabeth S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979453/
https://www.ncbi.nlm.nih.gov/pubmed/29601539
http://dx.doi.org/10.3390/ijms19041043
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author Rhett, J. Matthew
Yeh, Elizabeth S.
author_facet Rhett, J. Matthew
Yeh, Elizabeth S.
author_sort Rhett, J. Matthew
collection PubMed
description Over the past few decades, connexin hemichannels have become recognized as major players in modulating the inflammatory response. Chronic inflammation is documented to promote tumorigenesis and is a critical component of tumor progression. Furthermore, inflammation is strongly linked to angiogenesis, immunotolerance, invasiveness, metastasis, and resistance in breast cancers. In this review, the literature on the role of connexin hemichannels in inflammation is summarized, and the potential role for hemichannel-mediated inflammation in driving breast cancer progression is discussed. Lastly, the potential for connexin-based therapeutics to modulate the inflammatory component of the tumor microenvironment as an avenue for the treatment of breast cancer is also discussed.
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spelling pubmed-59794532018-06-10 The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response Rhett, J. Matthew Yeh, Elizabeth S. Int J Mol Sci Review Over the past few decades, connexin hemichannels have become recognized as major players in modulating the inflammatory response. Chronic inflammation is documented to promote tumorigenesis and is a critical component of tumor progression. Furthermore, inflammation is strongly linked to angiogenesis, immunotolerance, invasiveness, metastasis, and resistance in breast cancers. In this review, the literature on the role of connexin hemichannels in inflammation is summarized, and the potential role for hemichannel-mediated inflammation in driving breast cancer progression is discussed. Lastly, the potential for connexin-based therapeutics to modulate the inflammatory component of the tumor microenvironment as an avenue for the treatment of breast cancer is also discussed. MDPI 2018-03-30 /pmc/articles/PMC5979453/ /pubmed/29601539 http://dx.doi.org/10.3390/ijms19041043 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Rhett, J. Matthew
Yeh, Elizabeth S.
The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title_full The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title_fullStr The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title_full_unstemmed The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title_short The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response
title_sort potential for connexin hemichannels to drive breast cancer progression through regulation of the inflammatory response
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979453/
https://www.ncbi.nlm.nih.gov/pubmed/29601539
http://dx.doi.org/10.3390/ijms19041043
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