RETRACTED ARTICLE: Knockdown long non-coding RNA ANRIL inhibits proliferation, migration and invasion of HepG2 cells by down-regulation of miR-191

Deyu Huang,Chunhua Bi,Qingxi Zhao,Xueli Ding,Cheng Bian,Hui Wang,Ting Wang,Hua Liu

doi:10.1186/s12885-018-4831-6

Deyu Huang, Chunhua Bi + Show 6 more

Open Access

https://doi.org/10.1186/s12885-018-4831-6

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Abstract

BackgroundHepatocellular carcinoma (HCC) is a common malignant tumor with high fatality rate. Recent studies reported that up-regulation of long non-coding RNA antisense non-coding RNA in the INK4 locus (lncRNA ANRIL) was found in HCC tissues, and which could affect HCC cells biological processes. However, the potential molecular mechanism of ANRIL in HCC is still unclear. The study aimed to uncover the effect of ANRIL on HepG2 cells growth, migration and invasion.MethodsThe knockdown expression vectors of ANRIL were transfected into HepG2 cells, and qRT-PCR, CCK-8, flow cytometry, Transwell and western blot assays were performed to analyze the effect of ANRIL on cell proliferation, apoptosis, migration and invasion. The relative expression of miR-191 was then examined in ANRIL knockdown vector transfected cells. These experiments were repeated again for exploring the effect of miR-191 on HepG2 cells. NF-κB and Wnt/β-catenin signaling pathways were examined by using western blot assay.ResultsKnockdown of ANRIL inhibited proliferation, induced apoptosis, meanwhile suppressed migration and invasion of HepG2 cells. Additionally, the results showed that the expression level of miR-191 was down-regulated by ANRIL knockdown in HepG2 cells. Importantly, overexpression of miR-191 reversed the anti-tumor effect of ANRIL on cell proliferation, apoptosis, migration and invasion in HepG2 cells. Besides, we found that ANRIL knockdown inactivated NF-κB and Wnt/β-catenin pathways by regulating miR-191.ConclusionsThese data demonstrated that ANRIL knockdown suppressed proliferation, migration, invasion, and promoted apoptosis in HepG2 cells by down-regulating miR-191 and inactivating NF-κB and Wnt/β-catenin signaling pathways.

Highlights

Hepatocellular carcinoma (HCC) is a common malignant tumor with high fatality rate
We investigated the effect of antisense non-coding RNA in the INK4 locus (ANRIL) on HepG2 cells proliferation, apoptosis, migration and invasion, as well as uncovered whether ANRIL affected HCC cell biological processes through regulation of microRNA-191, nuclear factor kappa B (NF-κB) and Wnt/β-catenin signaling pathways
Knockdown of ANRIL suppressed cell proliferation and induced apoptosis in HepG2 cells To detect the effect of ANRIL on HCC cells proliferation and apoptosis, we first transfected the expression vectors of sh-ANRIL#1 and sh-ANRIL#2 into HepG2 cells to change ANRIL expression

Summary

Introduction

Hepatocellular carcinoma (HCC) is a common malignant tumor with high fatality rate. The potential molecular mechanism of ANRIL in HCC is still unclear. Hepatocellular carcinoma (HCC) is the commonest type of primary liver cancer, and is the main cause of death in patient with cirrhosis [1, 2]. Huang et al BMC Cancer (2018) 18:919 effective methods for the treatment of early HCC [4]. With the development of surgical and drug treatments, the 5-year survival rate of patients with HCC has obviously improved [5]. HCC remains a highly fatal cancer due to the lack of biomarkers and targets for early diagnosis [6]. The complex molecular mechanisms in the occurrence and development of HCC are still unclear. The effective molecular biomarkers are urgently needed for the diagnosis, treatment and prognosis of HCC

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