Search

Background: Multiple previous studies have indicated miR-516a-3p was associated with carcinogenesis in lung cancer. However, its biologic functions in lung adenocarcinoma remain unknown. The aim of this study was to investigate the expression of miR-516a-3p in lung adenocarcinoma, its molecular mechanisms of miR-516a-3p, and its effects on cell proliferation, migration, invasion, and apoptosis. Methods: The expression of miR-516a-3p and PTPRD was tested by reverse transcription-quantitative polymerase chain reaction. Cell migration and invasion assays were used to evaluate the migration and invasion ability of cells. Flow cytometry was performed to observe the effects of miR-516a-3p on the cell apoptosis. Western blot analysis was used to assess the protein levels of PTPRD. Luciferase reporter assay was utilized to identify whether PTPRD was a direct target of miR-516a-3p. Results: There was upregulated expression of miR-516a-3p in lung adenocarcinoma tissues as well as cell lines. In addition, miR-516a-3p expression knock-down could inhibit cell proliferation, invasion, and migration, but promote apoptosis in lung adenocarcinoma. By contrast, overexpression of miR-516a-3p resulted in the opposite effect. Dual luciferase assay, RT-PCR and western blot analysis results confirmed that PTPRD was a direct target for miR-516a-3p. Further studies also found PTPRD was down-regulated in lung adenocarcinoma and there was a negative correlation between miR-516a-3p and PTPRD expression in lung adenocarcinoma. Moreover, miR-516a-3p and PTPRD were significantly correlated with the clinical stage of lung adenocarcinoma. Conclusions: Our current findings showed that miR-516a-3p was up-regulated in lung adenocarcinoma, functioning as a tumor-promoting gene by targeting PTPRD.