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Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis

Autophagy is a lysosomal degradation process which is key for the regulation of the turnover of long-lived or damaged proteins and organelles and which promotes cell survival during nutrient deprivation or other microenvironmental stresses. Current evidence supports the hypothesis that autophagy sup...

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Detalles Bibliográficos
Autores principales: XU, YINGHUA, XIA, XIAOPING, PAN, HONGMING
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573143/
https://www.ncbi.nlm.nih.gov/pubmed/23420500
http://dx.doi.org/10.3892/ol.2012.1015
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author XU, YINGHUA
XIA, XIAOPING
PAN, HONGMING
author_facet XU, YINGHUA
XIA, XIAOPING
PAN, HONGMING
author_sort XU, YINGHUA
collection PubMed
description Autophagy is a lysosomal degradation process which is key for the regulation of the turnover of long-lived or damaged proteins and organelles and which promotes cell survival during nutrient deprivation or other microenvironmental stresses. Current evidence supports the hypothesis that autophagy suppresses tumorigenesis, particularly during the early stages of tumor initiation. However, in established tumors, autophagy promotes survival under stressful conditions during cancer progression and in response to chemotherapy; however, the mechanism by which autophagy influences cancer metastasis remains unknown. In this review, we discuss the capacity of an abnormal tumor environment to induce autophagy and consider how this relates to tumor metastasis and the attractive prospect of manipulating autophagic signaling pathways as potential targets for the treatment of cancer metastasis.
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spelling pubmed-35731432013-02-15 Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis XU, YINGHUA XIA, XIAOPING PAN, HONGMING Oncol Lett Review Autophagy is a lysosomal degradation process which is key for the regulation of the turnover of long-lived or damaged proteins and organelles and which promotes cell survival during nutrient deprivation or other microenvironmental stresses. Current evidence supports the hypothesis that autophagy suppresses tumorigenesis, particularly during the early stages of tumor initiation. However, in established tumors, autophagy promotes survival under stressful conditions during cancer progression and in response to chemotherapy; however, the mechanism by which autophagy influences cancer metastasis remains unknown. In this review, we discuss the capacity of an abnormal tumor environment to induce autophagy and consider how this relates to tumor metastasis and the attractive prospect of manipulating autophagic signaling pathways as potential targets for the treatment of cancer metastasis. D.A. Spandidos 2013-02 2012-11-07 /pmc/articles/PMC3573143/ /pubmed/23420500 http://dx.doi.org/10.3892/ol.2012.1015 Text en Copyright © 2013, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
XU, YINGHUA
XIA, XIAOPING
PAN, HONGMING
Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title_full Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title_fullStr Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title_full_unstemmed Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title_short Active autophagy in the tumor microenvironment: A novel mechanism for cancer metastasis
title_sort active autophagy in the tumor microenvironment: a novel mechanism for cancer metastasis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573143/
https://www.ncbi.nlm.nih.gov/pubmed/23420500
http://dx.doi.org/10.3892/ol.2012.1015
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