Dong Hao, Zhu Fengming, Jin Shilu, Tian Jing
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.
Exp Ther Med. 2020 Jul;20(1):205-210. doi: 10.3892/etm.2020.8707. Epub 2020 Apr 30.
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) 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.
炎症被认为是癌症的主要标志之一,且与胃癌相关。白细胞介素-22(IL-22)是IL-10家族的一员,在炎症性疾病和肿瘤中发挥重要作用。本研究的目的是检测IL-22对胃癌细胞(AGS细胞)增殖的影响,并探索相关的分子机制。使用转染了IL-22质粒的AGS细胞进行细胞计数试剂盒-8检测的结果表明,IL-22可促进AGS细胞活力。然而,当用IL-22短发夹(sh)RNA敲低IL-22时,AGS细胞的活力显著受损。蛋白质印迹结果表明,IL-22降低了丝裂原活化蛋白激酶(MAPK)信号通路的激活。此外,IL-22-shRNA转染增加了MAPK的激活,ERK和JNK磷酸化上调证明了这一点。综上所述,本研究结果表明,IL-22通过JNK信号通路调节胃癌细胞的活力,提示通过靶向IL-22治疗胃癌的方法。