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Chinese Journal of Clinical Oncology ; (24): 1007-1013, 2017.
Article in Chinese | WPRIM | ID: wpr-663371

ABSTRACT

Objective:Abnormal angiogenesis is an important hallmark of HCC. Ectopic miR-375 overexpression led to repression of proliferation, migration, invasion, and colony formation, and it induced apoptosis in hepatoma cells as well. In this study, we explored the effect of miR-375 on HCC angiogenesis. Methods:We evaluated the antiangiogenic effects of miR-375 using human umbilical vein endothelial cells, tube formation assays, rat aortic ring sprouting assays, and chicken chorioallantoic membrane assays. Bioinformatics software was used to predict the downstream target gene of miR-375. MiR-375 regulation to target genes was explored by overexpres-sion and knockdown of miR-375 in hepatoma cells. Luciferase assay was performed to confirm its molecular mechanism. Rescue assay of target gene was further used to prove that miR-375 inhibited HCC angiogenesis by directly regulating its target gene. Results:MiR-375 inhibited HCC angiogenesis. Platelet-derived growth factor-C (PDGFC) was a potential target gene of miR-375. MiR-375 inhibited PDGFC expression in hepatoma cells by targeting its 3′-UTR. MiR-375 exerted its antiangiogenic effect partially by PDGFC inhibition. Conclusion:MiR-375 repressed tumor angiogenesis by targeting PDGFC in HCC.

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