Abstract: Objective: To investigate the clinical significance and biological functions of serine/arginine- rich splicing factor 7 (SRSF7) expression in hepatocellular carcinoma (HCC). Methods: Firstly, the expression levels, clinical pathological features, functions, and pathway enrichment of SRSF7 were analyzed using HCC transcriptome and clinical data from TCGA database. Validation was then conducted using clinical HCC samples, Huh7, and Hep3B cell lines, which were divided into control group, overexpression group (SRSF7^OE group), and knockdown group (SRSF7^KD group). Proliferation and apoptosis abilities were assessed using cell counting kit-8 (CCK- 8) and TUNEL assays. Migration and invasion abilities were evaluated using wound healing, Transwell migration, and Transwell invasion assays. Epithelial-mesenchymal transition (EMT)- related markers’protein levels were determined by western blotting, while reverse transcription- quantitative PCR (RT-qPCR) was utilized to measure the mRNA levels of downstream regulatory genes of SRSF7. Results: Bioinformatics analysis revealed that SRSF7 was highly expressed in HCC tumor tissues and was associated with tumor grade, stage, and poor prognosis (P＜0.05). Western blotting and immunohistochemical results showed that SRSF7 was highly expressed in tumor tissues (P＜0.05). Compared with the control group, overexpression of SRSF7 promoted the proliferation, migration, invasion and EMT process of HCC cells; knockdown of SRSF7 could inhibit HCC cell proliferation, promote cell apoptosis, and inhibit HCC cell migration, invasion and EMT process (P＜0.05). Conclusion: SRSF7 is highly expressed in HCC, and its elevated expression may promote HCC cell proliferation and inhibit cell apoptosis by regulating the expression of downstream target genes such as PAK5 and RTL1, and promote cell migration and invasion by promoting EMT process, ultimately promoting HCC progression.