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A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer
Inflammation is a critical component of tumor progression, and it modifies the tumor microenvironment by various mechanisms. Here, we explore the effect of the inflammatory response on the tumor microenvironment in colorectal cancer (CRC). A prognostic signature consisting of inflammation-related ge...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10120913/ https://www.ncbi.nlm.nih.gov/pubmed/37014331 http://dx.doi.org/10.18632/aging.204630 |
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author | Li, Jinna Yang, Jiapeng Xing, Rui Wang, Ying |
author_facet | Li, Jinna Yang, Jiapeng Xing, Rui Wang, Ying |
author_sort | Li, Jinna |
collection | PubMed |
description | Inflammation is a critical component of tumor progression, and it modifies the tumor microenvironment by various mechanisms. Here, we explore the effect of the inflammatory response on the tumor microenvironment in colorectal cancer (CRC). A prognostic signature consisting of inflammation-related genes (IRGs) was constructed and verified based on the inflammatory response by bioinformatics analysis. IRG risk model was identified as an independent prognostic factor in CRC, and was related to biological processes of extracellular matrix, cell adhesion and angiogenesis. The IRG risk score predicted the clinical benefit of ipilimumab. Weighted correlation network analysis identified TIMP1 as the hub gene of the inflammatory response in the IRG risk model. Coculture experiments with macrophages and CRC cells revealed that TIMP1 promoted macrophage migration, inhibited the expression of M1 markers (CD11C and CD80), and promoted the expression of M2 markers (ARG1 and CD163). TIMP1 promoted the expression of ICAM1 and CCL2 by activating the ERK1/2 signaling pathway to promote macrophage migration and M2-like polarization. These IRGs in the risk model regulated stromal and immune components in the tumor microenvironment and could serve as potential therapeutic targets in CRC. TIMP1 promoted macrophage migration and meditated macrophage M2 polarization by activating ERK1/2/CLAM1 and CCL2. |
format | Online Article Text |
id | pubmed-10120913 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-101209132023-04-22 A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer Li, Jinna Yang, Jiapeng Xing, Rui Wang, Ying Aging (Albany NY) Research Paper Inflammation is a critical component of tumor progression, and it modifies the tumor microenvironment by various mechanisms. Here, we explore the effect of the inflammatory response on the tumor microenvironment in colorectal cancer (CRC). A prognostic signature consisting of inflammation-related genes (IRGs) was constructed and verified based on the inflammatory response by bioinformatics analysis. IRG risk model was identified as an independent prognostic factor in CRC, and was related to biological processes of extracellular matrix, cell adhesion and angiogenesis. The IRG risk score predicted the clinical benefit of ipilimumab. Weighted correlation network analysis identified TIMP1 as the hub gene of the inflammatory response in the IRG risk model. Coculture experiments with macrophages and CRC cells revealed that TIMP1 promoted macrophage migration, inhibited the expression of M1 markers (CD11C and CD80), and promoted the expression of M2 markers (ARG1 and CD163). TIMP1 promoted the expression of ICAM1 and CCL2 by activating the ERK1/2 signaling pathway to promote macrophage migration and M2-like polarization. These IRGs in the risk model regulated stromal and immune components in the tumor microenvironment and could serve as potential therapeutic targets in CRC. TIMP1 promoted macrophage migration and meditated macrophage M2 polarization by activating ERK1/2/CLAM1 and CCL2. Impact Journals 2023-04-02 /pmc/articles/PMC10120913/ /pubmed/37014331 http://dx.doi.org/10.18632/aging.204630 Text en Copyright: © 2023 Li et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Li, Jinna Yang, Jiapeng Xing, Rui Wang, Ying A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title | A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title_full | A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title_fullStr | A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title_full_unstemmed | A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title_short | A novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
title_sort | novel inflammation-related signature for predicting prognosis and characterizing the tumor microenvironment in colorectal cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10120913/ https://www.ncbi.nlm.nih.gov/pubmed/37014331 http://dx.doi.org/10.18632/aging.204630 |
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