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J BUON. 2019 Nov-Dec;24(6):2402-2410.

CircRNA_0000502 promotes hepatocellular carcinoma metastasis and inhibits apoptosis through targeting microRNA-124.

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Department of Hepatobiliary Surgery, Guizhou Provincial People's Hospital, Guiyang, China.



To investigate the expression level of circ_0000502 in hepatocellular carcinoma (HCC), and to further explore whether it can promote the malignant progression of HCC by targeting and binding to microRNA (miR)-124.


Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of circ_0000502 in 40 pairs of HCC tissue specimens and adjacent ones, and to analyze the relationship between circ_0000502 expression and prognosis of patients with HCC. QRT-PCR was used to verify the expression of circ_0000502 in HCC cells. The circ_0000502 knockdown model was constructed using lentivirus in HCC cell lines, and cell counting KIT-8 (CCK-8), Transwell and flow cytometry assays were used to figure out the effect of circ_0000502 on the function of HCC cells. Lastly, luciferase reporter gene assay was applied to verify the relationship between circ_0000502 and miR-124.


QRT-PCR results indicated that the level of circ_0000502 in HCC tissues was significantly higher than that in adjacent ones. Compared with patients with low expression of circ_0000502, patients with high expression of circ_0000502 had a lower overall survival rate compared with the negative control (NC) group. The proliferation, invasion and migration ability of circ_0000502 knockdown group significantly decreased, while on the contrary cell apoptosis increased. QRT-PCR results revealed that the expression of miR-124 and circ_0000502 mRNA in HCC tissues was negatively correlated. Also, the result of luciferase reporter gene assay demonstrated that circ_0000502 could be targeted by miR-124 via this binding site.


High expression of circ_0000502 was significantly positively correlated with poor prognosis of HCC. Besides, circ_0000502 promoted the malignant progression of HCC by regulating miR-124 expression.

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