1. Academic Validation
  2. IL-36G promotes cancer-cell intrinsic hallmarks in human gastric cancer cells

IL-36G promotes cancer-cell intrinsic hallmarks in human gastric cancer cells

  • Cytokine. 2022 Jul;155:155887. doi: 10.1016/j.cyto.2022.155887.
Ngan Le 1 Ian Luk 1 David Chisanga 2 Wei Shi 2 Lokman Pang 1 Glen Scholz 3 John Mariadason 1 Matthias Ernst 1 Jennifer Huynh 1
Affiliations

Affiliations

  • 1 Olivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, VIC, Australia.
  • 2 Olivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, VIC, Australia; School of Computing and Information Systems, The University of Melbourne, Parkville, VIC, Australia.
  • 3 Melbourne Dental School, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, VIC, Australia.
Abstract

Interleukin-36 gamma (IL-36G) is a member of the IL-36 subfamily of cytokines and acts as a potent driver of inflammation. IL-36G has been extensively characterized in the pathogenesis of psoriasis and has been recently described to play roles in wound healing particularly in the gastrointestinal tract. However, the effects of IL-36G during Cancer development including gastric Cancer remain unexplored. Here, we show that IL-36G induced ERK1/2 activation in AGS, MKN1 and MKN45 human gastric Cancer cell lines. Moreover, IL-36G induced colony formation, migration and invasion of these gastric Cancer cell lines that was inhibited by the natural antagonist, IL-36 receptor antagonist (RA). Interrogation of TCGA stomach adenocarcinoma patient datasets revealed highly elevated IL-36G gene expression in human gastric Cancer compared to normal tissue independent of tumor stage, and high IL-36G expression corresponded with poorer patient survival. Collectively, our results indicate for the first time that IL-36G supports a neoplastic phenotype in human gastric Cancer cells.

Keywords

Cytokines; Gastric cancer; IL-36G; Interleukins.

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