Objective To investigate the effects of microRNA-145(miR-145) on the proliferation and apoptosis of renal tubular epithelial cells and related mechanisms. Methods was transfected into renal tubular epithelial cells by lipofectamine 2000 reagent. The levels of miR-145 in renal tubular epithelial cells were detected by RT-PCR. The proliferation of cells was detected by CCK-8 assay. The distribution of cell cycle after transfection was detected by flow cytometry, and the expression levels of gastric cancer cells Bax, Cyclin B1, PCNA and Bcl-2 in stomach was detected by Western blot assay. The targeted relationship between miR-145 and PLK1 gene was reported using luciferin assases. Results RT-PCR assay showed that the expression level of miR-362 in renal tubular epithelial cells in the miR-145 transfection group was significantly higher than that in the control group (P＜0.05). Flow cytometry showed that there was no significant difference in G0/G1 phase ratio of renal tubular cells in each group (P＞0.05). The S-phase ratio of tubular cells in the miR-145 transfection group was (1416±282)%, which was significantly lower than that in the control group [(21.22±3.81)%] and the negative control group [(22.56±2.69)%] (P＜0.05). The G2/M phase ratio of tubular cells in the miR-145 transfection group was(26.37±4.51)%, which was significantly higher than that in the control group [(24.57±2.02)%] and the negative control group [(22.46±2.74)%] (P＜0.05). The relative level of Bax in miR-145 group was（0.36±0.04）, which was significantly higher than that in control group and negative control group (P＜0.05). The relative levels of Cyclin B1, PCNA and Bcl-2 in the miR-145 group were (0.18±0.03),(0.27±0.03) and (0.16±0.02), which were significantly lower than those in the control group (0.28±0.02), (0.36±0.04) and (0.32±0.03) and the negative control group (0.30±0.03), (0.40±0.03) and (0.33±0.03) (P＜0.05). Bioinformatics predictions showed that miR-145 could bind to the 3'-UTR of PLK1 gene. Luciferase reporter gene assay confirmed that the relative activity of luciferase in tubular cells decreased significantly after co-transfection of miR-145 and PLK1 wild-type vectors (P＜0.05). Luciferase activity in tubular cells of other experimental groups decreased significantly (P＜0.05). Relative activity did not decrease significantly (P＜0.05). RTPCR assay showed that PLK1 gene expression in renal tubular epithelial cells transfected with miR-145 was significantly lower than that in control group and negative control group. Conclusions The miR-145 can target the expression level of PLK1 gene in renal tubular epithelial cells, inhibit cell proliferation and induce cell apoptosis, providing experimental reference for the treatment of renal fibrosis.
