The incidence and mortality of gastric cancer have been increasing in recent years. MiR-126 and target genes have been studied in gastric cancer, but their studies with Golgi phosphoprotein 3 (GOLPH3) and related pathways in gastric cancer are rarely reported. In the present study, we aimed to investigate the interaction between the miR-126 and GOLPH3in the progression of gastric cancer. In this study, we revealed the role of miR-126-GOLPH3 axis into regulating the progression of epithelial-mesenchymal transition (EMT) in BGC-823 cell model. Firstly, tumor tissues and adjacent normal tissues were collected from 45 patients with gastric cancer. We found the expression of miR-126 in human tumor tissue was significantly lower than in normal tissue using reverse transcription-polymerase chain reaction (RT-PCR). But the GOLPH3 expression was opposite by the detection of immunohistochemistry, RT-PCR and Western blot. Moreover, we predicted miR-126 targeting GOLPH3 by bioinformatics and confirmed the interaction using luciferase reporter gene system; miR-126 inhibited the proliferation, invasion and EMT progression in BGC-823 cells through overexpressing miR-126; miR-126 negative regulated GOLPH3 expression by overexpressing and interfering miR-126. Finally, we found GOLPH3 could promote proliferation using MTT assay, invasion using Transwell, and EMT progression by inhibiting the expression of E-cadherin, inducing vimentin and N-cadherin in BGC-823 cells. Our results demonstrated that miR-126 inhibits proliferative and invasive ability as well as EMT progression by targeting GOLPH3. This study may provide a new field of vision for targeted treatment of gastric cancer.

近年来胃癌的发病率和死亡率一直在增加。在胃癌中已经对MiR-126和靶基因进行了研究，但很少报道它们与高尔基磷蛋白3（GOLPH3）及其相关途径有关的研究。在本研究中，我们旨在研究miR-126和GOLPH3在胃癌进展中的相互作用。在这项研究中，我们揭示了miR-126-GOLPH3轴在BGC-823细胞模型中调控上皮-间质转化（EMT）进程中的作用。首先，从45例胃癌患者中收集肿瘤组织和邻近的正常组织。我们发现，使用逆转录聚合酶链反应（RT-PCR），miR-126在人肿瘤组织中的表达明显低于正常组织。但是通过免疫组织化学，RT-PCR和Western印迹的检测，GOLPH3的表达是相反的。此外，我们通过生物信息学预测了miR-126靶向GOLPH3，并使用荧光素酶报告基因系统确认了相互作用。miR-126通过过度表达miR-126抑制BGC-823细胞的增殖，侵袭和EMT进程；miR-126通过过度表达和干扰miR-126负调控GOLPH3的表达。最后，我们发现GOLPH3可以通过抑制BGC-823细胞中E-钙粘蛋白的表达，诱导波形蛋白和N-钙粘蛋白的表达而使用MTT法促进增殖，使用Transwell侵袭和EMT进展。我们的结果表明，miR-126通过靶向GOLPH3抑制增殖和侵袭能力以及EMT进展。