Cargando…
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....
Autores principales: | , , , , |
---|---|
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 |
_version_ | 1783287961700270080 |
---|---|
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. |
format | Online Article Text |
id | pubmed-5739918 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT siposferenc relationoftheigfigf1rsystemtoautophagyincolitisandcolorectalcancer AT szekelyhajnal relationoftheigfigf1rsystemtoautophagyincolitisandcolorectalcancer AT kisimredaniel relationoftheigfigf1rsystemtoautophagyincolitisandcolorectalcancer AT tulassayzsolt relationoftheigfigf1rsystemtoautophagyincolitisandcolorectalcancer AT muzesgyorgyi relationoftheigfigf1rsystemtoautophagyincolitisandcolorectalcancer |