ELF3-AS1 promotes the carcinogenesis of hepatocellular carcinoma cells by inhibiting miR-98-5p/CPSF4 axis

Hepatocellular carcinoma (HCC), which predominantly manifests as a malignant form of primary liver cancer, remains resistant to existing therapies in many patients. Therefore, elucidating the cellular processes and signaling networks driving HCC progression and discovering novel treatment targets remain key areas of research. ELF3-AS1, miR-98-5p, and CPSF4 are closely associated with liver cancer, but the relationship between them is unclear. ELF3-AS1, miR-98-5p, and CPSF4 levels were quantified using RT-qPCR. CPSF4 expression was analyzed through Western blotting. Liver tumor cell viability was assessed using CCK8 assays. The metastatic potential of cells was primarily evaluated using wound healing and Transwell assays. ELF3-AS1’s impact on tumors was validated through live animal experiments by inducing subcutaneous tumor formation in nude mice. RNAhybrid and TargetScan analyzed potential miR-98-5p target regions in CPSF4 and ELF3-AS1. Our study demonstrates that reducing ELF3-AS1 expression can inhibit hepatoma cell proliferation, migration, and invasive abilities. Specifically, knocking down ELF3-AS1 can reduce the expression of CPSF4. Knocking down ELF3-AS1 can suppress liver cancer development in live animal models. In addition, miR-98-5p can bind ELF3-AS1 and CPSF4 and down-regulate the expression of CPSF4. In summary, ELF3-AS1 promotes the proliferation, migration, and invasion of HCC cells by inhibiting miR-98-5p/CPSF4 axis.