IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling

Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32α in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32α-Tg). In IL-32α-Tg mice, a...

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Autores principales: Yun, Hyung-Mun, Park, Kyung-Ran, Kim, Eun-Cheol, Han, Sang Bae, Yoon, Do Young, Hong, Jin Tae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496202/
https://www.ncbi.nlm.nih.gov/pubmed/25909160
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author Yun, Hyung-Mun
Park, Kyung-Ran
Kim, Eun-Cheol
Han, Sang Bae
Yoon, Do Young
Hong, Jin Tae
author_facet Yun, Hyung-Mun
Park, Kyung-Ran
Kim, Eun-Cheol
Han, Sang Bae
Yoon, Do Young
Hong, Jin Tae
author_sort Yun, Hyung-Mun
collection PubMed
description Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32α in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32α-Tg). In IL-32α-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32α increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32α and TNFR1 were increased. These findings indicate that IL-32α suppressed colon cancer development by promoting the death signaling of TNFR1.
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spelling pubmed-44962022015-07-10 IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling Yun, Hyung-Mun Park, Kyung-Ran Kim, Eun-Cheol Han, Sang Bae Yoon, Do Young Hong, Jin Tae Oncotarget Research Paper Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32α in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32α-Tg). In IL-32α-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32α increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32α and TNFR1 were increased. These findings indicate that IL-32α suppressed colon cancer development by promoting the death signaling of TNFR1. Impact Journals LLC 2015-04-13 /pmc/articles/PMC4496202/ /pubmed/25909160 Text en Copyright: © 2015 Yun et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Yun, Hyung-Mun
Park, Kyung-Ran
Kim, Eun-Cheol
Han, Sang Bae
Yoon, Do Young
Hong, Jin Tae
IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title_full IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title_fullStr IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title_full_unstemmed IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title_short IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
title_sort il-32α suppresses colorectal cancer development via tnfr1-mediated death signaling
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496202/
https://www.ncbi.nlm.nih.gov/pubmed/25909160
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