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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.

miR-126 targeting GOLPH3 inhibits the epithelial-mesenchymal transition of gastric cancer BGC-823 cells and reduces cell invasion