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.
IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
Hyung-Mun Yun,Kyung-Ran Park,Eun-Cheol Kim,S. Han,D. Yoon,J. Hong
Published 2015 in OncoTarget
ABSTRACT
PUBLICATION RECORD
- Publication year
2015
- Venue
OncoTarget
- Publication date
2015-04-13
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
CONCEPTS
- azoxymethane-induced colon cancer
A chemically induced mouse model of colon carcinogenesis generated by azoxymethane exposure.
Aliases: AOM-induced colon cancer, AOM-induced colon carcinogenesis
- il-32α
An isoform of the interleukin-32 cytokine studied in transgenic mice and colon cancer tissues.
Aliases: interleukin-32 alpha
- jnk activation
Activation of the c-Jun N-terminal kinase signaling pathway in cells.
Aliases: c-Jun N-terminal kinase activation
- reactive oxygen species production
Generation of oxidant molecules inside cells, used here as a measured signaling-related outcome.
Aliases: ROS production, ROS
- tnfr1
Tumor necrosis factor receptor 1, a cell-surface receptor involved in death-signaling pathways.
Aliases: tumor necrosis factor receptor 1
- tnfr1-mediated apoptosis
Programmed cell death triggered through TNFR1-dependent signaling.
Aliases: TNFR1-mediated cell death
REFERENCES
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