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Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer

Metabolic syndrome (MetS), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor (IGF1R) signaling pathway....

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Autores principales: Sipos, Ferenc, Székely, Hajnal, Kis, Imre Dániel, Tulassay, Zsolt, Műzes, Györgyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739918/
https://www.ncbi.nlm.nih.gov/pubmed/29290648
http://dx.doi.org/10.3748/wjg.v23.i46.8109
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author Sipos, Ferenc
Székely, Hajnal
Kis, Imre Dániel
Tulassay, Zsolt
Műzes, Györgyi
author_facet Sipos, Ferenc
Székely, Hajnal
Kis, Imre Dániel
Tulassay, Zsolt
Műzes, Györgyi
author_sort Sipos, Ferenc
collection PubMed
description Metabolic syndrome (MetS), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor (IGF1R) signaling pathway. The IGF1R pathway has been reported to regulate autophagy, as well, but sometimes through a bidirectional context. Targeting the IGF1R-autophagy crosstalk could represent a promising strategy for the development of new antiinflammatory and anticancer therapies, and may help for subjects suffering from MetS who are at increased risk of colorectal cancer. However, therapeutic responses to targeted therapies are often shortlived, since a signaling crosstalk of IGF1R with other receptor tyrosine kinases or autophagy exists, leading to acquired cellular resistance to therapy. From a pharmacological point of view, it is attractive to speculate that synergistic benefits could be achieved by inhibition of one of the key effectors of the IGF1R pathway, in parallel with the pharmacological stimulation of the autophagy machinery, but cautiousness is also required, because pharmacologic IGF1R modulation can initiate additional, sometimes unfavorable biologic effects.
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spelling pubmed-57399182017-12-30 Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer Sipos, Ferenc Székely, Hajnal Kis, Imre Dániel Tulassay, Zsolt Műzes, Györgyi World J Gastroenterol Review Metabolic syndrome (MetS), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor (IGF1R) signaling pathway. The IGF1R pathway has been reported to regulate autophagy, as well, but sometimes through a bidirectional context. Targeting the IGF1R-autophagy crosstalk could represent a promising strategy for the development of new antiinflammatory and anticancer therapies, and may help for subjects suffering from MetS who are at increased risk of colorectal cancer. However, therapeutic responses to targeted therapies are often shortlived, since a signaling crosstalk of IGF1R with other receptor tyrosine kinases or autophagy exists, leading to acquired cellular resistance to therapy. From a pharmacological point of view, it is attractive to speculate that synergistic benefits could be achieved by inhibition of one of the key effectors of the IGF1R pathway, in parallel with the pharmacological stimulation of the autophagy machinery, but cautiousness is also required, because pharmacologic IGF1R modulation can initiate additional, sometimes unfavorable biologic effects. Baishideng Publishing Group Inc 2017-12-14 2017-12-14 /pmc/articles/PMC5739918/ /pubmed/29290648 http://dx.doi.org/10.3748/wjg.v23.i46.8109 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
spellingShingle Review
Sipos, Ferenc
Székely, Hajnal
Kis, Imre Dániel
Tulassay, Zsolt
Műzes, Györgyi
Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title_full Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title_fullStr Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title_full_unstemmed Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title_short Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer
title_sort relation of the igf/igf1r system to autophagy in colitis and colorectal cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739918/
https://www.ncbi.nlm.nih.gov/pubmed/29290648
http://dx.doi.org/10.3748/wjg.v23.i46.8109
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