Comprehensive bioinformatics analysis of critical lncRNAs, mRNAs and miRNAs in non‑alcoholic fatty liver disease.

Abstract:

:Non‑alcoholic fatty liver disease (NAFLD) is the most common fatty liver disease in developed countries, in which fat accumulation in the liver is induced by non‑alcoholic factors. The present study was conducted to identify NAFLD‑associated long non‑coding RNAs (lncRNAs), mRNAs and microRNAs (miRNAs). The microarray dataset GSE72756, which included 5 NAFLD liver tissues and 5 controls, was acquired from the Gene Expression Omnibus database. Differentially expressed lncRNAs (DE‑lncRNAs) and mRNAs (DE‑mRNAs) were detected using the pheatmap package. Using the clusterProfiler package and Cytoscape software, enrichment and protein‑protein interaction (PPI) network analyses were conducted to evaluate the DE‑mRNAs. Next, the miRNA‑lncRNA‑mRNA interaction network was visualized using Cytoscape software. Additionally, RP11‑279F6.1 and AC004540.4 expression levels were analyzed by reverse transcription quantitative polymerase chain reaction. There were 318 DE‑lncRNAs and 609 DE‑mRNAs identified in the NAFLD tissues compared with the normal tissues. Jun proto‑oncogene, AP‑1 transcription factor subunit (JUN), which is regulated by AC004540.4 and RP11‑279F6.1, exhibited higher degree compared with other nodes in the PPI network. Furthermore, miR‑409‑3p and miR‑139 (targeting JUN) were predicted as PPI network nodes. In the miRNA‑lncRNA‑mRNA network, miR‑20a and B‑cell lymphoma 2‑like 11 (BCL2L11) were among the top 10 nodes. Additionally, BCL2L11, AC004540.4 and RP11‑279F6.1 were targeted by miR‑20a, miR‑409‑3p and miR‑139 in the miRNA‑lncRNA‑mRNA network, respectively. RP11‑279F6.1 and AC004540.4 expression was markedly enhanced in NAFLD liver tissues. These key RNAs may be involved in the pathogenic mechanisms of NAFLD.

journal_name

Mol Med Rep

authors

Wu H,Song X,Ling Y,Zhou J,Tao Z,Shen Y

doi

10.3892/mmr.2019.9931

subject

Has Abstract

pub_date

2019-04-01 00:00:00

pages

2649-2659

issue

4

eissn

1791-2997

issn

1791-3004

journal_volume

19

pub_type

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