CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665.

Background: Numerous studies have shown that circular RNAs (circRNAs) play vital roles in tumor progression. However, how circRNAs function in hepatocellular cancer (HCC) remains mostly unclear. Methods: We analyzed HCC circRNA expression via a microarray, and the expression of an upregulated circRNA, circABCC2, was detected. We next explored the function of circABCC2 in HCC via a series of experiments. We performed RNA immunoprecipitation (RIP) and luciferase assays to explore the competing endogenous RNA (ceRNA) function of circABCC2 in HCC. Results: qRT-PCR verified that circABCC2 was overexpressed in HCC. Inhibition of circABCC2 suppressed HCC cell proliferation and invasion, but promoted apoptosis. Luciferase assays and RIP showed that circABCC2 and ABCC2 could directly bind to miR-665 and that circABCC2 could regulate ABCC2 expression by sponging miR-665. Conclusions: In summary, circABCC2 regulates ABCC2 expression and HCC progression by sponging miR-665. circABCC2 could be used as a biomarker and therapeutic target in HCC.

circFBLIM1 act as a ceRNA to promote hepatocellular cancer progression by sponging miR-346.

BACKGROUD: Accumulating evidences indicate that circular RNAs (circRNAs), a class of non-coding RNAs, play important roles in tumorigenesis. However, the function of circRNAs in hepatocellular cancer (HCC) is largely unknown. METHODS: We performed circRNA microarrays to identify circRNAs that are aberrantly expressed in HCC tissues. Expression levels of a significantly upregulated circRNA, circFBLIM1, was detected by quantitative real-time PCR (qRT-PCR) in HCC cell lines and tissues. Then, we examined the functions of circFBLIM1 in HCC by cell proliferation, apoptosis, invasion and mouse xenograft assay. In addition, luciferase assay and RNA immunoprecipitation (RIP) assay were used to explore the miRNA sponge function of circFBLIM1 in HCC. RESULTS: Microarray analysis and qRT-PCR verified a circRNA termed circFBLIM1 that was upregulated in HCC tissues and cell lines. Knockdown of circFBLIM1 inhibited proliferation, invasion and promoted apoptosis in HCC. Via luciferase reporter assays, circFBLIM1 and FBLIM1 were observed to directly bind to miR-346. Subsequent experiments showed that circFBLIM1 and FBLIM1 regulated the expression of each other by sponging miR-346. CONCLUSIONS: Taken together, we conclude that circFBLIM1 may function as a competing endogenous RNA (ceRNA) to regulate FBLIM1 expression through sponging miR-346 to exert regulatory functions in HCC. circFBLIM1 may be a diagnostic biomarker and potential target for HCC therapy.