Background: Circular RNAs (circRNAs), a class of non-coding RNAs, has been proved as an essential driver of hepatocellular carcinoma (HCC) progression. However, the aim of this study is to explore the role of hsa_circ_0097009 (circ_0097009) in HCC progression.
Methods: Ki67 expression in HCC tissues was labeled and examined by IHC assay. Quantitative real-time PCR (qRT-PCR) was applied to assess the expression of circ_0097009, miR-568 and RING finger protein 38 (RNF38). Western blot assay was conducted to analyze protein expression. HCC cell colony formation, proliferation, migration, invasion, angiogenesis ability and apoptosis were determined by colony formation assay, 5-ethynyl-29-deoxyuridine (EdU) assay, wound healing assay, trans well assay, angiogenesis assay and flow cytometry. The interaction between circ_0097009 and miR-568 as well as miR-568 and RNF38 was probed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays.
Results: We found that circ_0097009 and RNF38 expressions were markedly higher, but miR-568 expression was significantly lower in HCC. Circ_0097009 knockdown blocked HCC cell cloning, proliferation, migration, invasion, angiogenesis and facilitated apoptosis. MiR-568 was a target of circ_0097009 in HCC cells. MiR-568 interference could attenuate the circ_0097009 knockdown-induced inhibition on HCC cells progress. MiR-568 depressed cell clonal formation, proliferation, migration, invasion, angiogenesis and promotion of apoptosis, by targeting RNF38, and RNF38 overexpression reversed the suppression of miR-568 in HCC cells. Also, circ_0097009 knockdown blocked tumor growth in vivoCONCLUSION: Together, this study indicated that the oncogenic function of circ_0097009 in HCC, and circ_0097009/miR-568/RNF38 axis was expected to be a novel therapeutic option for HCC patients (Tab. 1, Fig. 7, Ref. 33). Text in PDF www.elis.sk Keywords: circ_0097009, miR-568, RNF38, hepatocellular carcinoma.