<i>ELF3-AS1</i> promotes the carcinogenesis of hepatocellular carcinoma cells by inhibiting <i>miR-98-5p</i>/<i>CPSF4</i> 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. <i>ELF3-AS1</i>, <i>miR-98-5p</i>, and <i>CPSF4</i> are closely associated with liver cancer, but the relationship between them is unclear. <i>ELF3-AS1</i>, <i>miR-98-5p</i>, and <i>CPSF4</i> levels were quantified using RT-qPCR. <i>CPSF4</i> 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. <i>ELF3-AS1</i>’s impact on tumors was validated through live animal experiments by inducing subcutaneous tumor formation in nude mice. RNAhybrid and TargetScan analyzed potential <i>miR-98-5p</i> target regions in <i>CPSF4</i> and <i>ELF3-AS1</i>. Our study demonstrates that reducing <i>ELF3-AS1</i> expression can inhibit hepatoma cell proliferation, migration, and invasive abilities. Specifically, knocking down <i>ELF3-AS1</i> can reduce the expression of <i>CPSF4</i>. Knocking down <i>ELF3-AS1</i> can suppress liver cancer development in live animal models. In addition, <i>miR-98-5p</i> can bind <i>ELF3-AS1</i> and <i>CPSF4</i> and down-regulate the expression of <i>CPSF4</i>. In summary, <i>ELF3-AS1</i> promotes the proliferation, migration, and invasion of HCC cells by inhibiting <i>miR-98-5p</i>/<i>CPSF4</i> axis.