Up-regulated RFC2 predicts unfavorable progression in hepatocellular carcinoma

BACKGROUND: Replication factor C (RFC) is closely related to tumor progression and metastasis. However, the functional significance of RFC2 in hepatocellular carcinoma remains unclear. MATERIALS AND METHODS: In order to solve this problem, the expression of RFC2 in liver cancer patients was analyzed through ONCOMINE, UALCAN, Human Protein Atlas. Survival analysis was conducted using Kaplan–Meier plotter and GEPIA. GO and KEGG enrichment analyses were carried out. The protein–protein interaction (PPI) network was performed through Metascape. Western blotting, cell counting kit-8 and transwell assay were used to detect the effect of RFC2 on cell proliferation and migration. RESULTS: The transcription and protein level of RFC2 in HCC were overexpressed, which was significantly related to the clinical individual cancer stage and pathological tumor grade of HCC patients. In addition, in patients with liver cancer, higher RFC2 expression was found to be significantly correlated with shorter OS and DFS. Furthermore, the function of RFC2 in liver cancer was DNA replication, and its main mechanism was the phase transition of the cell cycle. Biological experiments demonstrated that knockdown of RFC2 reduced the proliferation and migration of HCC cells. CONCLUSION: RFC2 might promote the development of liver cancer, which might be achieved by regulating cell cycle and DNA replication. It could be used as a novel biomarker for the prognosis of liver cancer. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s41065-021-00179-9.