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.