Aim
Increasing evidences show that microRNAs are engaged in hepatocellular carcinoma (HCC). The aim of this study was to investigate the role of miR-502-3P in HCC and to identify its underlying mechanism.
Conclusion
Taken together, overexpression of miR-502-3P or downregulation of SET may prove beneficial as a therapeutic strategy for HCC treatment.
Methods
The expression levels of miR-502-3P were assessed in multiple HCC cell lines and in liver tissues of patients with HCC. We further examined the effects of miR-502-3P on malignant behavior of HCC. The molecular target of miR-502-3P was identified using a computer algorithm and confirmed experimentally.
Results
Downregulation of miR-502-3P was found in both HCC cell lines and human samples. Overexpression of miR-502-3P dramatically inhibits HCC proliferation, metastasis, invasion, and cell adhesion. We further verify the SET as a novel and direct target of miR-502-3P in HCCs.