MiR-616 plays oncogenic role in hepatocellular carcinoma progression through suppressing PTEN expression and activating PI3K/AKT pathway

Abstract Aims: Given their regulatory roles in gene expression, microRNAs play an important role in tumorigenesis. The current study aimed to explore the function and the related mechanisms of miR-616 in hepatocellular carcinoma (HCC). Methods: The expression of miR-616 was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Chi-square test was applied to estimate the association of miR-616 with clinical characteristics of HCC patients. Cell transfection was performed by Lipofectamine？ 2000. MTT assay was used to detect cell proliferation, whereas cell motility was estimated using Transwell assay. The protein expression was detected using western blot. Results: MiR-616 was significantly up-regulated in HCC tissues and cells (p？<？.05 for all). Moreover, its elevated expression was positively correlated with lymph node metastasis (p？=？.008) and TNM stage (p？=？.012). Knockdown of miR-616 resulted in decreased cell proliferation, migration and invasion. Moreover, the inhibition of miR-616 significantly suppressed PI3K/AKT pathway. The bioinformatics analysis and luciferase reporter assay suggested that PTEN was a targeted gene of miR-616. PTEN had the capacity to reverse the oncogenic function of miR-616 in HCC. Conclusion: MiR-616 activates PI3K/AKT pathway through suppressing PTEN expression, thus promoting the progression of HCC