Reverses Multidrug Resistance by Targeting miR-212/Trim14 in Gastric Cancer Cells

Abstract

Aim: To investigate the role of miR-212/Trim14 in the chemoresistance of gastric cancer cells. Methods: Both the SGC7901-MDR (drug-resistant gastric cancer cells) and SGC7901 (drug-sensitive gastric cancer cells) cells was used. Cell viability was measured using cell counting kit-8 (CCK-8). Quantitative Real-time PCR (QRT-PCR) and Western blot were used to detect the expression levels of miR-212 and Trim14 in GC tissues and cells. The targeting relationship between miR-216a-5p and HMGB1 was verified through bioinformatics website prediction and double luciferase reporter gene experiment. Apoptosis was detected by flow cytometry. Finally, the migration and invasion abilities of the cells were tested by transwell and wound scoring experiments. Results: The miR-212 overexpression increased the chemosensitivity of SGC7901-MDR cells to 5-FU, cisplatin, and docetaxel, and decreased chemical resistance SGC7901-MDR cells to chemotherapy drugs. Trim14 is the target gene of miR-212, and in vitro experiments showed that overexpression of miR-212 promoted apoptosis of GC cells and inhibited the migration and invasion of SGC7901-MDR cells. Up-regulation of Trim14 promoted the reversal of the above effects. Conclusions: Our results indicated that miR-212 overexpression reversed multidrug resistance in GC cells by promoting apoptosis and targeting Trim14.