The novel circRNA hsa_circ_0000038 inhibits the progression of hepatocellular carcinoma by sponging miR-92a-2-5p to regulate the p53/p21 proteins

Abstract Background The abnormal regulation of circular RNA (circRNA) levels is commonly identified in human diseases, particularly malignant tumors. Recently, the diagnostic value of circRNAs has received increased attention. The detailed mechanisms of various cancer and circular RNAs need more research to clarify, including hepatocellular carcinoma HCC.Methods We utilized quantitative real-time fluorescence polymerase chain reaction (RT-qPCR) to measure the expression level of hsa_circ_0000038 in paired hepatocellular carcinoma (HCC) and adjacent noncancerous liver tissues. GO annotation and enrichment analysis were used to examine the potential downstream pathways. RT-qPCR and western blotting were conducted to evaluate the expression of the p53/p21pathway. CCK-8, wound closure, and Transwell assays were used to measure cell proliferation, migration, and invasion. Luciferase and chromatin immunoprecipitation assays were used to investigate the interactions between miR-92a-2-5p and hsa_circ_0000038.Results Levels of hsa_circ_0000038 were downregulated in HCC tissues and cells. Overexpression of hsa_circ_0000038 inhibited tumor growth in vivo and blocked the hepatocarcinoma cell cycle at the G0–G1 phase and repressed cell proliferation, invasion, and migration of HCC cells in vitro, while co-transfection of miR‐92a-2‐5p partially attenuated the effects mediated by hsa_circ_0000038. The expression of miR-92a-2-5p was decreased in HCC tissues and promoted cell proliferation and the cell cycle in vitro. hsa_circ_0000038 acted as a sponge for miR-92a-2-5p, and Tp53 gene was the target of miR-92a-2-5p. Hsa_circ_0000038 inhibited the progression of tumor growth by inhibiting the miR-92a-2-5p/p53/p21 axis.Conclusion Our study reveals aberrant circRNA expression profiles in HCC tissues. Hsa_circ_0000038 regulates the miR-92a-2-5p/p53/p21 axis and be involved in HCC development.