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

ABSTRACT: Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32? in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32?-Tg). In IL-32?-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-mediated apoptosis was increased. Also, IL-32? increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32? and TNFR1 were increased. These findings indicate that IL-32? suppressed colon cancer development by promoting the death signaling of TNFR1.

SUBMITTER: Yun HM

PROVIDER: S-EPMC4496202 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

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

Yun Hyung-Mun HM Park Kyung-Ran KR Kim Eun-Cheol EC Han Sang Bae SB Yoon Do Young DY Hong Jin Tae JT

Oncotarget 20150401 11

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-mediated apoptosis was increased. Also, IL-32α increased ROS production to induce prolonged JNK ac ...[more]

PMID: 25909160

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