miR‑25 expression is upregulated in pancreatic ductal adenocarcinoma and promotes cell proliferation by targeting ABI2

MicroRNAs (miRNAs) are reported to play a critical role in the regulation of cancer cell proliferation; however, the role of microRNA-25 (miR-25) in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In the present study, the role of miR-25 in PDAC cell proliferation was investigated. Upregulated expression of miR-25 was found in PDAC tissues and cell lines by reverse transcription-quantitative PCR. Cell proliferation was significantly enhanced by overexpression of miR-25 as shown by CCK-8 assay results. Meanwhile, overexpression of miR-25 also promoted G1-to-S phase transition of the cell cycle in Aspc-1 cells via flow cytometry analysis. However downregulation of miR-25 inhibited the tumor cell proliferation and cell cycle transition. Online software was used to predict the target gene for miR-25 and luciferase reporter assay confirmed that Abl interactor 2 (ABI2) was a target of miR-25 via direct binding of its 3' untranslated region with miR-25. Moreover, results of the western blot analysis demonstrated that miR-25 negatively regulated the expression of ABI2 at the protein level. In addition, introduction of ABI2 mRNA into cells overexpressing miR-25 attenuated the carcinogenic effects of miR-25. In conclusion, these findings demonstrate that miR-25 plays an oncogenic role and promotive role in PDAC cell proliferation via targeting of ABI2.