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Micro RNA ‐3178 ameliorates inflammation and gastric carcinogenesis promoted by H elicobacter pylori new toxin, Tip‐α, by targeting TRAF 3
Author(s) -
Zou Meijuan,
Wang Fang,
Jiang Aiqin,
Xia Anliang,
Kong Siya,
Gong Chun,
Zhu Mingxia,
Zhou Xin,
Zhu Jun,
Zhu Wei,
Cheng Wenfang
Publication year - 2017
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12348
Subject(s) - transfection , proinflammatory cytokine , inflammation , microrna , cancer , downregulation and upregulation , carcinogenesis , apoptosis , biology , cancer research , helicobacter pylori , microbiology and biotechnology , immunology , chemistry , cell culture , biochemistry , genetics , gene
Background Helicobacter pylori infection is the main cause of chronic gastritis, peptic ulcer, and gastric cancer. Tip‐ α is a newly identified carcinogenic factor present in H. pylori . TRAF 3 can activate NF ‐κB by both canonical and noncanonical signaling pathways. In this study, we found that the expression of TRAF 3 and NF ‐κB was upregulated, while microRNA‐3178 (miR‐3178) was decreased in H. pylori ‐positive gastric tissues but not in H. pylori ‐negative tissues. Materials and Methods GES ‐1 cells were incubated with 12.5 μg/mL recombinant Tip‐α ( rT ip‐α) in RPMI 1640 for 2 hours. After another 24 hours, the supernatant medium was designed as inflammatory‐conditioned medium ( ICM ) and that from the untreated control cells was designed as untreated control medium. The release of proinflammatory cytokines from GES ‐1 cells and proliferation of gastric cancer cells was determined by ELISA and CCK ‐8 kits. Cells were transfected with the mimic, inhibitor, negative control of miR‐3178, or TRAF 3 si RNA control si RNA . The medium was then replaced with RPMI 1640, 12.5 μg/mL rT ip‐α, and collected, and the total cellular RNA and protein were extracted for the following detection. Results MiR‐3178 mimic prevented the increasement of TRAF 3 and hence decreased activation of NF ‐κB signals, whereas miR‐3178 inhibitor could not, in GES ‐1 cells with Tip‐α treatment. The condition medium from miR‐3178 mimic transfected GES ‐1 cells could inhibit proliferation and induce apoptosis of inflammation‐related gastric cancer cells SGC 7901 and MGC 803 by decreasing the production of inflammatory cytokines TNF ‐α and IL ‐6, which were secreted by GES ‐1 cells. Conclusions Taken all together, Tip‐α might activate NF ‐κB to promote inflammation and carcinogenesis by inhibiting miR‐3178 expression, which directly targeting TRAF 3, during H. pylori infection in gastric mucosal epithelial cells.