LncRNA ASB16-AS1 Promotes Growth And Invasion Of Hepatocellular Carcinoma Through Regulating miR-1827/FZD4 Axis And Activating Wnt/β-Catenin Pathway
Authors Yao X, You G, Zhou C, Zhang D
Received 22 June 2019
Accepted for publication 11 October 2019
Published 7 November 2019 Volume 2019:11 Pages 9371—9378
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Chien-Feng Li
Xiaoxiao Yao,1,* Guangqiang You,1,* Chen Zhou,2 Dan Zhang1
1Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Jilin University, Changchun 130041, People’s Republic of China; 2Personnel Department, The First Affiliated Hospital of Jilin University, Changchun 130000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Dan Zhang
Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Jilin University, No. 218 Ziqiang Street, Nanguan District, Changchun 130041, People’s Republic of China
Background: To date, although several long noncoding RNAs (lncRNAs) are reported to regulate hepatocellular carcinoma (HCC) development, their relationship still remains elusive. ASB16-AS1 is a poorly researched novel lncRNA. We aimed to investigate its function in HCC progression.
Methods: qRT-PCR and in situ hybridization (ISH) were used to analyze ASB16-AS1 expression in HCC tissues. CCK8, Edu incorporation and colony formation were used to determine cell proliferation. Transwell assay was used to examine migration and invasion. Luciferase reporter assay was used to analyze the interactions among ASB16-AS1, miR-1827 and FZD4.
Results: Bioinformatics analysis identified ASB16-AS1 was overexpressed in HCC tissues, which was further validated by qRT-PCR and in situ hybridization (ISH). Besides, ASB16-AS1 was demonstrated to be a potential indicator for HCC prognosis. Functional studies showed ASB16-AS1 knockdown attenuated proliferation, migration and invasion of HCC cells. Mechanistically, ASB16-AS1 directly interacted with miR-1827 and promoted FZD4 expression by sponging miR-1827. Overexpressed FZD4 eventually activated Wnt/β-catenin pathway and contributed to HCC progression.
Conclusion: Our work is the first to identify ASB16-AS1 as an oncogene that enhances HCC progression by modulating miR-1827/FZD4/Wnt/β-catenin pathways.
Keywords: lncRNA, HCC, ASB16-AS1, miR-1827, FZD4
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