MicroRNA‑300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β‑catenin signaling
- Jinping Bai
- Yingchun Gao
- Yanhui Du
- Xue Yang
- Xinye Zhang
Affiliations: School of Clinical Medicine, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China, Quality Control Office, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin 130000, P.R. China, Department of Geriatrics, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin 130000, P.R. China, Department of Thyroid Head and Neck Surgery, Jilin Cancer Hospital, Changchun, Jilin 130033, P.R. China, Nursing College, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China
- Published online on: August 5, 2019 https://doi.org/10.3892/ol.2019.10712
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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. In vitro 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.