目的:探讨miR-29c 调控TNRC18 胃癌组织和细胞阿帕替尼耐药性的机制。方法：收集2015 年2 月至2017 年10 月武汉市中心医院具有完整资料的39 例胃癌和癌旁组织标本（其中21 例为阿帕替尼耐药患者、18 例为不耐药患者），采用qRT-PCR检测miR-29c 在胃癌组织和细胞系中的表达水平。采用CCK-8、Transwell 和Annexin V-FITC/PI 双染流式术检测miR-29c 过表达/敲降对MGC-803/AP耐药细胞增殖、侵袭和凋亡影响，Western blotting 检测miR-29c 调控TNRC18 表达，双荧光素酶报告基因验证miR-29c 与TNRC18 的靶向作用关系。结果：miR-29c 在3 种胃癌细胞系和阿帕替尼耐药癌患者组织中均低表达。双荧光素酶报告基因证实miR-29c 靶向作用TNRC18 并下调其表达水平。miR-29c 通过靶向下调TNRC18 抑制阿帕替药耐药的MGC-803/AP细胞的增殖、侵袭并促进细胞凋亡（均P<0.05 或P<0.01)，进而降低胃癌细胞MGC-803/AP对阿帕替尼的耐药性。体内实验同样证实，miR-29c 通过靶向抑制TNRC18 降低胃癌对阿帕替尼的耐药性。结论：miR-29c/TNRC18 分子轴在胃癌组织和细胞MGC-803/AP对阿帕替尼耐药中发挥着一定作用，过表达miR-29c可逆转MGC-803/AP细胞对阿帕替尼耐药。

Objective: To investigate the mechanism of miR-29c modulating apatinib resistance of gastric cancer tissues and cells MGC-803 via regulating TNRC18. Methods: A total of 39 gastric cancer patients with complete clinical data, who were treated in the Central Hospital of Wuhan from Feb. 2015 to Oct. 2017, were collected for this study. The expression of miR-29c was detected by qRTPCR in gastric cancer tissues and cell lines. The effect of miR-29c over-expression/knockdown on the proliferation, invasion and apoptosis of MGC-803/AP cells in vitro was measured by CCK-8 assay, Transwell and Annexin V-FITC/PI double staining flow cytometry assay. Western blotting was used to detect the regulation of miR-29c on TNRC18. Moreover, the relationship between miR-29c and TNRC18 was examined by dual luciferase reporter gene assay. Results: qRT-PCR revealed that miR-29c was low expressed in gastric cancer cell lines and gastric cancer tissues from patients resistant to apatinib. Moreover, dual luciferase reporter gene assay confirmed that miR-29c directly binds to the 3′ UTR of TNRC18 mRNA to suppress its expression in MGC-803/AP cells. Furthermore, miR-29c inhibited the apatinib resistance in gastric cancer MGC-803/AP cells via inhibiting cell proliferation, invasion and promoting cell apoptosis by targeted down-regulating TNRC18. Additionally, in vivo experiment also confirmed that miR-29c modulated apatinib-resistance in gastric cancer cells by targeted inhibiting TNRC18. Conclusion: miR-29c/TNRC18 axis plays a certain role in the resistance of gastric cancer tissues and MGC-803/AP cells to apatinib, and over-expression of miR-29c may reverse the resistance of MGC-803/AP cells to apatinib.