Aim
In this paper, we aim to investigate the underlying mechanism by which miR-325-3p regulate the progression of HCC.
Conclusion
MiR-325-3p regulated angiogenesis of HCC via mediating CXCL17/CXCR8 axis, indicating miR-325-3p may serve as a promising therapy biomarker for HCC.
Methods
RT-qPCR was performed to detect the levels of miR-325-3p, CXCL17, and CXCR8. Western bolt was conducted to determine the levels of pro-angiogenic factors VEGF, FGF2, Ang-1 and PDGF-B. Immunohistochemistry was carried to detect the distribution and expression of Ki-67 and CD34 in HCC tissues. MTT and colony formation were carried to evaluate cell proliferation, endothelial tube-formation assay was used detect tubule formation, and transwell assay was performed to evaluate cell migration and invasion ability. Dual-luciferase activity assay was used to verify the relationship between miR-325-3p and CXCL17.
Results
MiR-325-3p was down-regulated in HCC cells and tissues, miR-325-3p overexpression inhibited the proliferation, migration and invasion of HCC cells. Besides, miR-325-3p overexpression inhibited angiogenesis of HCC. CXCL17 is a direct target of miR-325-3p and partially mediates the effect of miR-325-3p on proliferation, migration, invasion and angiogenesis of HCC.