MicroRNA‑296 targets AKT2 in pancreatic cancer and functions as a potential tumor suppressor.

Although microRNA-296 (miR-296) has been studied in various types of human cancer, its expression, biological role and mechanism of action in pancreatic cancer remains to be elucidated. The aim of the current study was to investigate the expression level, possible roles and underlying molecular mechanisms of miR‑296 in pancreatic cancer. The present study revealed that miR‑296 is significantly downregulated in tissue from patients with pancreatic cancer and in human pancreatic carcinoma cell lines, when compared with matched healthy tissue and normal human pancreatic cell lines, respectively. In addition, restoration of miR‑296 expression was revealed to inhibit the proliferation, migration and invasive activity of pancreatic cancer cells. Furthermore, bioinformatics analysis and a luciferase reporter assay validated the AKT2 gene as a direct target of miR‑296 in pancreatic cancer. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis revealed that miR‑296 was able to decrease AKT2 expression at the post‑transcriptional level. Notably, the effects of AKT2 knockdown were similar to miR‑296 overexpression in pancreatic cancer. In conclusion, the present findings indicate a role for miR‑296 as a tumor suppressor in pancreatic cancer through directly targeting AKT2, thus suggesting that miR‑296 may serve as a potential therapeutic target for the treatment of pancreatic cancer.