MiR-188-3p and miR-133b Suppress Cell Proliferation in Human Hepatocellular Carcinoma via Post-Transcriptional Suppression of NDRG1. (5th August 2021)

• Record Type: Journal Article
• Authors: Luo, Zhenzhao; Fan, Yue; Liu, Xianchang; Liu, Shuiyi; Kong, Xiaoyu; Ding, Zhonghuan; Li, Ying; Wei, Liqing
• Is Part Of: Technology in cancer research & treatment. Volume 20(2021)
• Publication Date: 2021-08-05
• Subjects: hepatocellular carcinoma -- miR-188-3p -- miR-133b -- N-myc downstream regulated gene 1; Oncology -- Periodicals; Cancer -- Diagnosis -- Periodicals; Cancer -- Treatment -- Technological innovations -- Periodicals; 616.994
• DOI: 10.1177/15330338211033074
• Languages: English
• ISSNs: 1533-0346

Abstract

Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce apoptosis of cancer cells. However, the molecular mechanism of NRDG1 involved in hepatocellular carcinoma (HCC) tumorigenesis is still unknown. Methods: The expressions of miR-188-3p, miR-133b, and NRDG1 in HCC tissues and cells were quantified by qRT-PCR and Western blot. MTT assay and transwell invasion assay were performed to evaluate cell growth and cell migration, respectively. Luciferase reporter assay were performed to determine whether miR-188-3p and miR-133b could directly bind to NRDG1 in HCC cells. Results: The results showed that NRDG1 was upregulated and these 2 microRNAs were downregulated in HCC tissues. NRDG1 was negatively correlated with miR-188-3p and miR-133b in HCC tissues. MiR-188-3p and miR-133b were demonstrated to directly bind to 3′UTR of NRDG1 and inhibit its expression. Upregulation of miR-188-3p and miR-133b reduced NRDG1 expression in hepatocellular carcinoma cell lines, which consequently inhibited cell growth and cell migration. Conclusions: Our finding suggested that miR-188-3p and miR-133b exert a suppressive effect on hepatocellular carcinoma proliferation, invasion, and migration through downregulation of NDRG1.