Abstract: Objective To explore the effect and molecular mechanism of lncRNA RAB11B-AS1 on gastric cancer cell proliferation, migration, invasion and cisplatin sensitivity. Methods The cisplatin-resistant gastric cancer cells (HGC-27/DDP) were divided into control group, si-NC group, and si-RAB11B-AS1 group; tetra-methylazolium salt colorimetric assay(MTT) was used to detect cell survival rate; real-time fluorescence quantitative PCR (RT-qPCR) was applied to detect the expressions of RAB11B-AS1 and miR-628-3p; flow cytometry was used to detect cell cycle; cell migration and invasion were examined by Transwell cell method and dual luciferase report experiment was applied to detect the targeting relationship between RAB11B-AS1 and miR-628-3p. Results The survival rate of HGC-27 cells was significantly reduced after 0.2 and 0.4 mg/L cisplatin treatment (P＜0.05), but the survival rate of HGC-27/DDP cells after 0-0.4 mg/L cisplatin treatment was not statistically changed. The expression of RAB11B-AS1 in HGC-27 andHGC-27/DDP cells was significantly increased (P＜0.05), and the expression of RAB11B-AS1 in HGC-27/DDP cells was significantly higher than that of HGC-27 cells (P＜0.05). Interfering with the expression of lncRNA RAB11B-AS1, the proportion of G₀-G₁ phase cells was increased significantly, the proportion of S phase cells was decreased significantly (P＜0.05). Both cell survival rate and the number of migrating and invasive cells were significantly reduced (P＜0.05). RAB11B-AS1 was found to specifically regulate miR-628-3p. Conclusions LncRNA RAB11B-AS1 can inhibit the proliferation, migration and invasion of gastric cancer cells by up-regulating the expression of miR-628-3p, and increase the sensitivity of cancer cells to cisplatin.

Key words: lncRNA RAB11B-AS1, miR-628-3p, gastric cancer, proliferation, cisplatin, sensitivity