IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling
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Hyung-Mun Yun1,*, Kyung-Ran Park1,*, Eun-Cheol Kim1, Sang Bae Han2, Do Young Yoon3, Jin Tae Hong2
1Department of Maxillofacial Tissue Regeneration, School of Dentistry and Research Center for Tooth & Periodontal Regeneration (MRC), Kyung Hee University, Seoul 130-701, Republic of Korea
2College of Pharmacy and Medical Research Center, Chungbuk National University, Heungduk-gu, Cheongju, Chungbuk 361-763, Republic of Korea
3Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Seoul 150-716, Republic of Korea
*These authors have contributed equally to this work
Jin Tae Hong, e-mail: firstname.lastname@example.org
Keywords: IL-32α, colon cancer, TNFR1, RIP1
Received: January 01, 2015 Accepted: January 25, 2015 Published: April 13, 2015
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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