MicroRNA-300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β-catenin signaling.

A number of studies have demonstrated that altered expression levels of microRNA-300 (miR-300) are associated with tumor progression; however, little is understood regarding the role of miR-300 in hepatocellular carcinoma (HCC). The present study aimed to investigate the expression, biological function and potential regulatory mechanism of miR-300 in HCC. A miR-300 mimic and miR-300 inhibitor were transfected into liver cancer cells using RNAiMAX reagent. The expression levels of miR and mRNA were detected by reverse transcription-quantitative polymerase chain reaction. Protein expression levels were detected by western blot analysis. Cell growth was determined using Cell Counting Kit-8, a colony formation assay and cell cycle assay. miRNA targeting sites were analyzed using bioinformatics analysis and dual-luciferase reporter assay. The results revealed that miR-300 expression was significantly decreased in HCC tissues and cell lines. experiments demonstrated that overexpression of miR-300 could inhibit cell proliferation, colony formation and cell cycle progression of liver cancer cells. By contrast, inhibition of miR-300 was associated with increased rates of cell proliferation, colony formation and cell cycle progression. Notably, regulation of nuclear pre-mRNA domain-containing protein 1B (CREPT) was identified as a putative target gene of miR-300 by bioinformatics analysis. A luciferase reporter assay revealed that miR-300 directly targets the 3'-untranslated region of CREPT. Further data demonstrated that miR-300 can regulate CREPT expression levels in liver cancer cells. Notably, miR-300 was identified to regulate the Wnt/β-catenin signaling pathway in liver cancer cells. The restoration of CREPT expression partially reversed the antitumor effect of miR-300. In conclusion, the current results revealed a tumor suppressive role of miR-300 in HCC and indicated that the underlying mechanism was associated with a regulation of CREPT. The present study suggests that miR-300 and CREPT may serve as potential therapeutic targets for liver cancer.