CircMCM7 Promotes Hepatocellular Carcinoma Cell Proliferation and Metastasis By Modulating MCM7 Expression.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally. Although advanced progress has been made in recent years, the prognosis remains unsatisfactory, and new biomarkers are urgently needed for improved diagnosis and treatment. In this work, the Gene Expression Omnibus (GEO) database was screened to identify the novel circular RNA circMCM7, and its expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Actinomycin D treatment and RNase R assay were performed to examine the stability of circMCM7. CCK-8 assay and 5-ethynyl-2'-deoxyuridine (EdU) staining were used to detect the proliferation of HCC cells following sh-circMCM7 transfection. Annexin V-fluorescein isothiocyanate (FITC) staining was performed to determine the apoptosis rate. Transwell assay was employed to evaluate the invasion rate. Finally, the anti-tumor effect was verified through in vivo experiments, with proliferation and apoptosis assessed by immunohistochemistry (IHC) staining for Ki67 and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, respectively. Our results demonstrated that circMCM7 was highly expressed in HCC tumor tissues, and elevated circMCM7 expression was correlated with poor clinical outcomes in HCC patients. The closed-loop structure of circMCM7 conferred greater stability compared to linear GAPDH mRNA. Knockdown of circMCM7 significantly suppressed HCC cell proliferation and invasion while promoting apoptosis. Minichromosome maintenance complex component 7 (MCM7), a DNA replication marker, was also upregulated in HCC. Notably, overexpression of MCM7 partially rescued the inhibitory effects on proliferation and invasion, as well as the pro-apoptotic effects induced by circMCM7 knockdown. This study elucidates the oncogenic function of circMCM7 in hepatocellular carcinoma and confirms its regulatory roles in HCC cell proliferation, invasion, and apoptosis through modulation of MCM7 expression, suggesting circMCM7 as a potential therapeutic target for HCC treatment.