Interleukin-22 regulates gastric cancer cell proliferation through regulation of the JNK signaling pathway

Experimental and Therapeutic Medicine
Hao DongJing Tian

Abstract

Inflammation is considered as one of the major hallmarks of cancer and is associated with gastric cancer. Interleukin-22 (IL-22), a member of the IL-10 family, serves an important role in inflammatory diseases and tumors. The aim of the present study was to examine the effects of IL-22 on the proliferation of gastric cancer cells (AGS cells) in vitro and explore the associated molecular mechanism. The results of a Cell Counting kit-8 assay using AGS cells transfected with an IL-22-plasmid indicated that IL-22 could promote AGS cell viability. However, when IL-22 was knocked down by IL-22-short hairpin (sh)RNA, the viability of AGS cells was significantly impaired. Western blotting results indicated that IL-22 decreased the activation of the mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, IL-22-shRNA transfection increased the activation of MAPK, as evidenced by the upregulated phosphorylation of ERK and JNK. Taken together, the results of the present study suggest that IL-22 regulated the viability of gastric cancer cells through the JNK signaling pathway, suggesting a therapeutic approach for gastric cancer via targeting IL-22.

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Citations

Jun 3, 2021·International Journal of Molecular Sciences·Sana HibinoKoji Taniguchi
Nov 7, 2021·Gastric Cancer : Official Journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association·Karolina Kaźmierczak-SiedleckaKarol Połom

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Datasets Mentioned

BETA
GES-1

Methods Mentioned

BETA
protein assay
transfection
flow cytometry

Software Mentioned

Image
Pro Plus
SPSS

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