ABSTRACT
Objective:To investigate the expression of miRNA-522-3p (miR-522-3p) in gastric cancer tissues/cells and its regulation of RSU1 expression and to analyze the effect of miR-522-3p on biological function of gastric cancer cells in vitro.Methods:miR-522-3p relative expression levels in tumor tissues and adjacent tissues of 50 patients clinically diagnosed as gastric cancer in Shanxi Bethune Hospital from May 2019 to June 2019 were detected by using real-time quantitative polymerase chain reaction (qRT-PCR). MGC-803 cells and BGC-823 cells in gastric cancer were divided into miR-522-3p inhibitor group (transfected with miR-522-3p inhibitor) and empty vector group (transfected with empty vector). The cell proliferation was detected by using CCK-8 assay, cell scratch assay was used to detect the scratch healing ability of cells, and flow cytometry was used to detect the apoptosis. The target correlation between miR-522-3p and RSU1 was detected by using double luciferase reporter gene assay, the change of RSU1 protein was detected by using Western blot.Results:qRT-PCR showed that compared with adjacent cancer tissues, the relative expression level of miR-522-3p was up-regulated, and the difference was statistically significant (0.84±0.31 vs. 0.48±0.22, t = 2.93, P < 0.05). There were no statistically significant differences in the relative expression level of miR-522-3p in gastric cancer tissues with different tumor diameter and pathological grade (all P < 0.05). In vitro experimental assay showed that the cell proliferation rates of MGC-803 and BGC-823 cells in miR-522-3p inhibitor group at 48 h and 72 h were decreased (all P < 0.05). Furthermore, MGC-803 and BGC-823 tranfected with miR-522-3p inhibitor could effectively inhibit the scratch healing ability of MGC-803 and BGC-823 cells. Dual-luciferase reporter gene assay verified that miR-522-3p targeted to RSU1 3'UTR and affected its fluorescence activity. Western blot results showed that miR-522-3p could promote RSU1 protein expression. Conclusions:miR-522-3p is involved in the progression of gastric cancer probably via the regulation of RSU1 expression, and it may be a potential therapeutic target.