目的：探讨miR-361-5p对胃癌SGC-7901细胞奥沙利铂（oxaliplatin，OXA）耐药性的影响及其作用机制。方法：采用qPCR法检测miR-361-5p在胃癌细胞MKN-45、MGC80-3、SGC-7901和OXA耐药细胞SGC-7901/OXA中的表达水平。利用脂质体转染技术分别将 miR-361-5p mimics/inhibitor、sh-CCND1 转染到 SGC-7901/OXA 细胞中 ，用 CCK-8 法和流式细胞术检测SGC-7901/OXA细胞的增殖、凋亡和细胞周期。用双荧光素酶报告基因实验验证miR-361-5p与CCND1的靶向关系，用WB法检测 CCND1 的表达水平。结果：miR-361-5p 在多种胃癌细胞和 SGC-7901/OXA 细胞中均低表达（P<0.05 或 P<0.01）。过表达miR-361-5p可显著促进SGC-7901/OXA细胞凋亡，诱导G0/G1细胞周期停滞并抑制细胞增殖（P<0.05或P<0.01）。双荧光素酶报告基因实验结果证实，miR-361-5p靶向负调控CCND1的表达（P<0.01）。敲减CCND1抑制SGC-7901/OXA细胞CCND1表达和细胞增殖，并诱导凋亡和G0/G1周期阻滞（P<0.05或P<0.01）。过表达miR-361-5p靶向下调CCND1进而促进SGC-7901/OXA细胞凋亡，诱导G0/G1细胞周期停滞并抑制细胞增殖（P<0.05或P<0.01）。结论：miR-361-5p过表达可逆转胃癌SGC-7901/OXA细胞对OXA的耐药性，其机制可能与靶向下调CCND1表达有关。

Objective: To investigate the effects of miR-361-5p on the oxaliplatin (OXA) resistance of gastric cancer SGC-7901 cells and its mechanism. Methods: The expression of miR-361-5p in gastric cancer cells (MKN-45, MGC80-3 and SGC-7901) and drugresistant SGC-7901/OXA cells was detected by qPCR. The SGC-7901/OXA cells were transfected with miR-361-5p mimics/inhibitor or sh-CCND1 by using Liposome transfection technology. Then, cell proliferation, apoptosis and cell cycle of SGC-7901/OXA cells were measured by CCK-8 assay and Flow cytometry, respectively. The targeting relationship between miR-361-5p and CCND1 was examined by Dual luciferase report gene assay. The expression level of CCND1 in SGC-7901/OXA cells was detected by WB.Results: miR-361-5p was down-regulated in multiple gastric cancer cells and SGC-7901/OXA cells (P<0.05 or P<0.01). Over-expression of miR-361-5p significantly promoted the apoptosis, induced G0/G1 cell cycle arrest and inhibited cell proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Dual luciferase reporter gene results verified that miR-361-5p targeted CCND1 and negatively regulated its expression (P<0.01). Further experiments showed that targeted down-regulation of CCND1 induced apoptosis and G0/G1 cell cycle arrest and inhibited CCND1 expression and proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Over-expression of miR-361-5p targetedly down-regulated CCND1 and further promoted cell apoptosis, induced G0/G1 cell cycle arrest and inhibited cell proliferation of SGC-7901/OXA cells (P<0.05 or P<0.01). Conclusion: miR-361-5p over-expression can reverse the resistance of SGC-7901/OXA cells to OXA, and the mechanism may be related to its targeted down-regulation of CCND1 expression.