Hepatocellular carcinoma (HCC) is a kind of malignant tumor derived from hepatocytes and hepatobiliary cells, and its occurrence is prevalent worldwide. Although medical technology is developing rapidly, the therapeutic efficacy of HCC is still poor. Emerging evidence manifests that microRNAs (miRNAs) play a crucial role in various cancers and have been regarded as cancer suppressor gene. However, the regulatory mechanisms mediated by miR-647 involved in HCC remain unclear. Hence, to clarify the regulatory mechanisms mediated by miR-647 in HCC, we studied the independent effects of miR-647 and explored protein tyrosine phosphatase receptor type F (PTPRF) in the constructed HCC cell line (HCV-huh7.5). Thereafter, we used dual-luciferase gene reporting and Western blot to investigate the relationship between PTPRF and miR-647. Furthermore, we studied the mechanism of miR-647 on PTPRF in HCV-huh7.5. We found that miR-647 could not only promote the proliferation and invasion of HCV-huh7.5 cells but also facilitate cell migration, while PTPRF has the opposite effect. Besides, the results of cell function experiment implied that the overexpression of miR-647 or inhibition of PTPFRF remarkably influenced the Erk signaling pathway, which could regulate cell proliferation, migration, and invasion. In addition, the dual luciferase reporting identified PTPRF as a direct target of miR-647. We further demonstrated that miR-647 inhibitor or PTPRF knockdown administration boosted HCV-huh7.5 cell proliferation, migration, and invasion by targeting PTPRF.These findings provided clues for the mechanism of miR-647 in promoting the biology of HCV-huh7.5 cells by inhibiting the expression level of PTPRF.
Keywords: Erk1/2; PTPRF; hepatocellular carcinoma; miR-647.