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

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 experi-ment. 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 inva-sion 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 apop-tosis and targeting Trim14.