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Revisiting autophagy addiction of tumor cells

Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported t...

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Autores principales: Nyfeler, Beat, Eng, Christina H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4990994/
https://www.ncbi.nlm.nih.gov/pubmed/27097231
http://dx.doi.org/10.1080/15548627.2016.1170265
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author Nyfeler, Beat
Eng, Christina H.
author_facet Nyfeler, Beat
Eng, Christina H.
author_sort Nyfeler, Beat
collection PubMed
description Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported to depend on macroautophagy in order to cope with oncogene-induced metabolic stress. Our recent report details the unexpected finding that autophagy is dispensable for KRAS-driven tumor growth in vitro and in vivo. Additionally, we clarify that the antitumorigenic effects of chloroquine, a frequently used nonspecific inhibitor of autophagy, are not connected to the inhibition of macroautophagy. Our data suggest that caution should be exercised when using chloroquine and its analogs to decipher the roles of autophagy in cancer.
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spelling pubmed-49909942016-08-25 Revisiting autophagy addiction of tumor cells Nyfeler, Beat Eng, Christina H. Autophagy Autophagic Puncta Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported to depend on macroautophagy in order to cope with oncogene-induced metabolic stress. Our recent report details the unexpected finding that autophagy is dispensable for KRAS-driven tumor growth in vitro and in vivo. Additionally, we clarify that the antitumorigenic effects of chloroquine, a frequently used nonspecific inhibitor of autophagy, are not connected to the inhibition of macroautophagy. Our data suggest that caution should be exercised when using chloroquine and its analogs to decipher the roles of autophagy in cancer. Taylor & Francis 2016-04-20 /pmc/articles/PMC4990994/ /pubmed/27097231 http://dx.doi.org/10.1080/15548627.2016.1170265 Text en © 2016 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Autophagic Puncta
Nyfeler, Beat
Eng, Christina H.
Revisiting autophagy addiction of tumor cells
title Revisiting autophagy addiction of tumor cells
title_full Revisiting autophagy addiction of tumor cells
title_fullStr Revisiting autophagy addiction of tumor cells
title_full_unstemmed Revisiting autophagy addiction of tumor cells
title_short Revisiting autophagy addiction of tumor cells
title_sort revisiting autophagy addiction of tumor cells
topic Autophagic Puncta
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4990994/
https://www.ncbi.nlm.nih.gov/pubmed/27097231
http://dx.doi.org/10.1080/15548627.2016.1170265
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