IL-32a 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-32a in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32a-Tg). In IL-32a-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32a increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32a and TNFR1 were increased. These findings indicate that IL-32a suppressed colon cancer development by promoting the death signaling of TNFR1.