CircZFR promotes hepatocellular carcinoma progression through regulating miR-3619-5p/CTNNB1 axis and activating Wnt/ß-catenin pathway.

ABSTRACT

Circular RNAs (circRNAs) have been discovered to exert essential roles in human cancers, including hepatocellular carcinoma. Although circZFR has been reported to facilitate the growth of papillary thyroid cancer, the role of circZFR in hepatocellular carcinoma (HCC) are largely unknown. In this study, bioinformatics analysis showed that circZFR was closely related with hepatocellular carcinoma. We then detect the expression of circZFR in HCC tissues using qRT-PCR. Furthermore, Kaplan-Meier method and log rank test revealed that high expression of circZFR was associated with the poor prognosis of patients with HCC. Subsequently, loss-of-function assay indicated that circZFR knockdown significantly suppressed cell proliferation and epithelial-mesenchymal transition (EMT) in HCC. In addition, microarray analysis was utilized to identify the differentially expressed mRNAs in response to circZFR knockdown. Moreover, Gene Ontology (GO) analysis further showed that circZFR might regulate Wnt/ß-catenin signaling pathway. The results were further confirmed by luciferase reporter assay and western blot assays. Then bioinformatics tools predicted that cicrZFR enhanced the CTNNB1 expression via sponging miR-3619-5p. In summary, our findings indicated that circZFR may exert carcinogenic role in HCC through regulating miR-3619-5p/CTNNB1 axis and activating Wnt/ß-catenin pathway. These findings may provide a novel perspective for the treatment of hepatocellular carcinoma.