Abstract
BackgroundA growing body of evidence indicates that long non-coding RNAs (lncRNAs) can act as competitive endogenous RNAs (ceRNAs) to bind to microRNAs (miRNAs), thereby affecting and regulating the expression of target genes. The lncRNA–miRNA–mRNA ceRNA network has been theorized to play an indispensable role in many types of tumors. However, the role of the lncRNA-related ceRNA regulatory network in lung adenocarcinoma (LUAD) remains unclear.MethodsWe downloaded the RNAseq and miRNAseq data of LUAD from The Cancer Genome Atlas (TCGA) data portal and identified differentially expressed lncRNAs (DElncRNAs), differentially expressed miRNAs (DEmiRNAs), and differentially expressed mRNAs (DEmRNAs) between LUAD and corresponding paracancerous tissues by using the edgeR package of R software. We constructed the lncRNA–miRNA–mRNA ceRNA network by using Cytoscape (version 3.7.2) on the basis of the interaction generated from the miRcode, miRTarBase, miRDB, and TargetScan databases. Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed with DAVID 6.8 bioinformatics resources and plotted by using the ggplot2 package in R. The effect of genes on LUAD prognosis was assessed by applying the survival package in R in accordance with the Kaplan–Meier curve.ResultsIn total, 1645 DElncRNAs, 117 DEmiRNAs, and 2729 DEmRNAs were identified in LUAD. The LUAD-specific ceRNA network was composed of 157 nodes and 378 edges (329 DElncRNA–DEmiRNA interactions and 49 DEmiRNA–DEmRNA interactions). GO and KEGG pathway annotations suggested that the LUAD-specific ceRNA network was related to tumor-related molecular functions and pathways. Seven lncRNAs (DISC1-IT1, SYNPR-AS1, H19, LINC00460, LINC00518, DSCR10, and STEAP2-AS1), one miRNA (hsa-mir-31), and 16 mRNAs (ATAD2, OSCAR, KIF23, E2F7, PFKP, MCM4, CEP55, CBX2, CCNE1, CLSPN, CCNB1, CDC25A, EZH2, CHEK1, SLC7A11, and PBK) were revealed to be significantly correlated with overall survival.ConclusionIn this study, we described the potential regulatory mechanism of the progression of LUAD. We proposed a new lncRNA–miRNA–mRNA ceRNA network that could help further explore the molecular mechanisms of LUAD.
Highlights
Lung cancer is one of the most frequent cancers worldwide [1]
The top 10 DElncRNAs, DEmiRNAs, and differentially expressed mRNAs (DEmRNAs) with their names, log2FC values, and P-values are listed in Supplementary Table 1
LncRNA TTN-AS1 is overexpressed in lung adenocarcinoma (LUAD) compared with that in paracancerous tissues, and its overexpression can promote the malignant development of LUAD by regulating the miR-1425p/cyclin-dependent kinase 5 signaling pathway [22]
Summary
Lung cancer is one of the most frequent cancers worldwide [1]. It is classified into small cell lung carcinoma (accounting for 15% of cases) and non-small cell lung carcinoma (NSCLC, accounting for 85% of cases) [2]. NSCLC is further divided into three types: lung adenocarcinoma (LUAD), squamous cell carcinoma, and large cell carcinoma; LUAD is the main histological subtype of lung cancer and accounts for 40% of all cases [3]. Despite advances in diagnosis and treatment in recent years, the overall survival rate of patients with LUAD remains unsatisfactory. The lncRNA– miRNA–mRNA ceRNA network has been theorized to play an indispensable role in many types of tumors. The role of the lncRNA-related ceRNA regulatory network in lung adenocarcinoma (LUAD) remains unclear
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