Interleukin‑22 regulates gastric cancer cell proliferation through regulation of the JNK signaling pathway
- Hao Dong
- Fengming Zhu
- Shilu Jin
- Jing Tian
Affiliations: Department of Clinical Medicine, Binzhou Medical University, Binzhou, Shandong 256603, P.R. China, Tendering Office, Binzhou People's Hospital Affiliated to Binzhou Medical University, Binzhou, Shandong 256610, P.R. China, Department of Digestive Internal Medicine, Binzhou People's Hospital Affiliated to Binzhou Medical University, Binzhou, Shandong 256610, P.R. China, Department of Digestive Internal Medicine, Zouping People's Hospital, Binzhou, Shandong 256600, P.R. China
- Published online on: April 30, 2020 https://doi.org/10.3892/etm.2020.8707
Copyright: © Dong
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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.