Home Neoplasma 2018 Neoplasma Vol.65, No.5, p.753-761, 2018

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.65, No.5, p.753-761, 2018

Title: MiR-589-5p is a potential prognostic marker of hepatocellular carcinoma and regulates tumor cell growth by targeting MIG-6
Author: M. Xu, Y. Wang, H.T. He, Q. Yang

Abstract: MicroRNAs (miRNAs) are small noncoding RNAs approximately with 22 nucleotides. Accumulating evidence indicates that they are involved in carcinogenesis and tumor progression and recent investigations have also reported that several microRNAs can act as biomarkers in cancer diagnosis and prognosis. MicroRNA-589-5p (miR-589-5p) is a less studied microRNA, and herein we examined its roles in hepatocellular carcinoma (HCC). We analyzed miR-589-5p expression in HCC tissues by sequencing data and proved its expression in liver cancer cell lines by quantitative real-time PCR (qRT-PCR). We then studied its effect on liver cancer cell growth by MTT assay, colony formation and flow cytometry, and identified its target gene by luciferase reporter assay. We found that miR-589-5p was commonly over-expressed in HCC specimens. High expression of miR-589-5p was a risk factor for HCC patients (Hazard ratio [HR] = 1.434; 95% confidence intervals [CI] = 1.006-2.044; p = 0.046). We also found miR-589-5p had higher expression in the HepG2 and HuH-7 hepatocarcinoma cell lines than in the normal Lo-2hepatocyte. We established that suppression of miR-589-5p inhibited cell proliferation and cell cycle progression by loss-of-function studies. Furthermore, we found mitogen-inducible gene 6 (MIG-6) is a target for miR-589-5p. Our study demonstrated that miR-589-5p facilitated the growth of liver cancer cells by targeting MIG-6 and that it could be a prognosis biomarker for HCC. Suppression of miR-589-5p may be a feasible approach for inhibiting HCC progress.

Keywords: hepatocellular carcinoma, microRNA-589-5p, prognosis, MIG-6
Published online: 24-Sep-2018
Year: 2018, Volume: 65, Issue: 5 Page From: 753, Page To: 761

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