Downregulation of long non-coding RNA MEG3 promotes proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-β1.

Abstract:

:Hepatocellular carcinoma is a common malignant cancer with high incidence. And long non-coding RNAs (lncRNAs) play pivotal roles in the development of different types of cancers. In this study, we aimed to investigate the role of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of hepatocellular carcinoma. Expression of MEG3 in tumor tissues and adjacent healthy tissues of hepatocellular carcinoma patients, as well as the serum of both hepatocellular carcinoma patients and healthy controls, was detected by quantitative reverse transcriptase-polymerase chain reaction. The results showed that expression level of MEG3 was significantly lower in tumor tissues than in adjacent healthy tissues. Serum level of MEG3 was also significantly lower in hepatocellular carcinoma patients than in normal controls. The receiver operating characteristic curve analysis was used to evaluate the diagnostic value of MEG3 for hepatocellular carcinoma, and the prognostic value of MEG3 for this disease was analyzed using Kaplan-Meier method. The results indicated that serum level of MEG3 was a diagnostic and prognostic marker for hepatocellular carcinoma. We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-β inhibitor treatment reduced those enhancing effects. MEG3 siRNA silencing also increased the expression level of TGF-β1. These results indicated that downregulation of MEG3 can promote proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-β1 expression.

authors

Dong H,Zhang Y,Xu Y,Ma R,Liu L,Luo C,Jiang W

doi

10.1093/abbs/gmz046

subject

Has Abstract

pub_date

2019-06-20 00:00:00

pages

645-652

issue

6

eissn

1672-9145

issn

1745-7270

pii

5488704

journal_volume

51

pub_type

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