BMB Reports 2019; 52(3): 165-174  https://doi.org/10.5483/BMBRep.2019.52.3.019
Interleukin-32: Frenemy in cancer?
Sora Han1 & Young Yang2,*
1Research Institute for Women’s Health, 2Department of Biological Sciences, Sookmyung Women’s University, Seoul 04310, Korea
Correspondence to: Tel: +82-2-710-9590; Fax: +82-2-2077-7322; E-mail: yyang@sookmyung.ac.kr
Received: November 19, 2018; Published online: March 31, 2019.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Interleukin-32 (IL-32) was originally identified in natural killer (NK) cells activated by IL-2 in 1992. Thus, it was named NK cell transcript 4 (NK4) because of its unknown function at that time. The function of IL-32 has been elucidated over the last decade. IL-32 is primarily considered to be a booster of inflammatory reactions because it is induced by proinflammatory cytokines and stimulates the production of those cytokines and vice versa. Therefore, many studies have been devoted to studying the roles of IL-32 in inflammationassociated cancers, including gastric, colon cancer, and hepatocellular carcinoma. At the same time, roles of IL-32 have also been discovered in other cancers. Collectively, IL-32 fosters the tumor progression by nuclear factor-κB (NF-κB)-mediated cytokines and metalloproteinase production, as well as stimulation of differentiation into immunosuppressive cell types in some cancer types. However, it is also able to induce tumor cell apoptosis and enhance NK and cytotoxic T cell sensitivity in other cancer types. In this review, we will address the function of each IL-32 isoform in different cancer types studied to date, and suggest further strategies to comprehensively elucidate the roles of IL-32 in a contextdependent manner.
Keywords: Apoptosis, Cancer stem cell (CSC), Inflammatory cancer, Interleukin 32 (IL-32), Natural killer (NK) cell, Women’s cancer
Figures
Fig. 1. Biological functions of IL-32 in inflammatory tumors. Different colors indicate each cancer type and cancer type specific signaling pathway. AOM: azoxymethane, ROS: reactive oxygen species, JNK: c-Jun N-terminal kinases, NF-κB: nuclear factor kappa B, TIMP: tissue inhibitors of metalloproteinase, MMP: matrix metalloproteinase, H. pylori: Helicobacter pylori, cagPAI: cytotoxin-associated gene pathogenicity island, HBV: hepatitis B virus, HCV: hepatitis C virus, VEGF: vascular endothelial growth factor, CXCL: C-X-C motif chemokine, CCL: C-C motif chemokine ligands, TNF-α: tumor necrosis factor α, PI3K: phosphoinositide 3-kinase, AP-1: activated protein 1.


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