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.
Keywords: Hepatocellular carcinoma; MiR-616; PI3K/AKT; PTEN.