Hsa_circ_0007991 Promotes Immune Evasion in Hepatocellular Carcinoma via Regulation of the miR-505-3p/CANX Axis.

OBJECTIVE: This study aimed to investigate the expression and functional role of hsa_circ_0007991 in hepatocellular carcinoma (HCC). METHODS: RNA expression data of HCC and corresponding non-tumor liver tissues were obtained from the GEO database, and differential expression analysis was conducted to identify significantly dysregulated circRNAs. A total of 68 clinical samples from HCC patients were collected, and hsa_circ_0007991 level was quantified using RT-qPCR. Gain- and loss-of-function experiments were performed on HCC cells, followed by assessments of cellular proliferation, apoptosis, and immune evasion using CCK-8, EdU incorporation assays, flow cytometry, and ELISA. The role of hsa_circ_0007991 as a ceRNA was further validated using dual-luciferase reporter assay, RNA immunoprecipitation, and nuclear-cytoplasmic fractionation. RESULTS: A significant upregulation of hsa_circ_0007991 was observed in HCC tissues, with increased levels correlating with advanced TNM stages. hsa_circ_0007991 silencing significantly suppressed HCC cell proliferation and immune evasion, while promoting apoptosis, whereas hsa_circ_0007991 overexpression yielded the opposite effects. The function of hsa_circ_0007991 involves binding to miR-505-3p, which modulates the expression of calnexin (CANX), influencing the biological behaviors of HCC cells. Rescue experiments validated the essential function of the hsa_circ_0007991/miR-505-3p/CANX pathway in HCC. CONCLUSION: hsa_circ_0007991 is upregulated in HCC and closely associated with tumor proliferation and immune evasion by regulating the miR-505-3p/CANX axis.