Abstract
OBJECTIVES: Hepatocellular carcinoma (HCC) mostly developsfrom cirrhosis, so we compared the miRNA profiles of patients with cirrhosis who developed HCC with those who did not, and screened for miR-145-5p, which may be involved in the progression of liver cancer. The study's purpose was to explore the mechanism of miR-145-5p in cirrhosis that becomes HCC. METHODS: Cell counting kit 8 (CCK-8) and clone formation assays were employed to calculate cell proliferative ability. Quantitative real-time PCR (qRT-PCR) was conducted to measure the mRNA levels of miR-145-5p, plasminogen activator inhibitor 1 (PAI-1), and Circular RNA PVT1 (circPTV1). RESULTS: MiR-145-5p was downregulated in HCC, and miR-145-5p inhibited Huh-7 cell viability and clone formation. The Area Under the Curve (AUC) of miR-145-5p for distinguishing between the HCC and Tumor-free groups was 0.900, indicating a high diagnostic accuracy. PAI-1 was identified as a downstream target of miR-145-5p. Silencing PAI-1 decreased the viability and clone formation of Huh-7 cells. circPVT1 directly binding to miR-145-5p in HuH-7 cells. circPVT1 regulates cell viability and clone formation through miR-145-5p. In summary, we identified miRNA miR-145-5p, which was lowly expressed in HCC, and inhibited the viability and clone formation of HCC cells. CONCLUSION: Our research elucidates the regulatory role of the circPVT1/miR-145-5p/PAI-1 axis in HCC, suggesting its potential as a novel diagnostic biomarker or therapeutic target for HCC.