Identification of dysregulated long non-coding RNAs/microRNAs/mRNAs in TNM I stage lung adenocarcinoma
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Ziqiang Tian1, Shiwang Wen1, Yuefeng Zhang1, Xinqiang Shi1, Yonggang Zhu1, Yanzhao Xu1, Huilai Lv1 and Guiying Wang2
1Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China
2The Second Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China
Guiying Wang, email: firstname.lastname@example.org
Keywords: TNM I stage, lung adenocarcinoma, long non-coding RNA, microRNA, RNA-sequencing
Received: December 29, 2016 Accepted: May 06, 2017 Published: June 16, 2017
Lung adenocarcinoma (LUAD) is the primary subtype in lung cancer, which is the leading cause of cancer-related death worldwide. This study aimed to investigate the aberrant expression profiling of long non-coding RNA (lncRNA) in TNM I stage (stage I) LUAD. The lncRNA/mRNA/miRNA expression profiling of stage I LUAD and adjacent non-tumor tissues from 4 patients were measured by RNA-sequencing. Total of 175 differentially expressed lncRNAs (DELs), 1321 differentially expressed mRNAs (DEMs) and 94 differentially expressed microRNAs (DEMIs) were identified in stage I LUAD. DEMI-DEM regulatory network consisted of 544 nodes and 1123 edge; miR-200 family members had high connectivity with DEMs. In DEL-DEM co-expression network, CDKN2B-AS1, FENDRR and LINC00312 had the high connectivity with DEMs, which co-expressed with 105, 63 and 61 DEMs, respectively. DEL-DEMI-DEM network depicted the links among DELs, DEMI and DEMs. Identified DEMs were significantly enriched in cell adhesion molecules, focal adhesion and tight junction of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways; and enriched in cell adhesion, angiogenesis and regulation of cell proliferation of Gene Ontology biological processes. Quantitative real-time polymerase chain reaction results were generally consistent with our bioinformatics analyses. LINC00312 and FENDRR had diagnostic value for LUAD patients in The Cancer Genome Atlas database. Our study might lay the foundation for illumination of pathogenesis of LUAD and identification of potential therapeutic targets and novel diagnosis biomarkers for LUAD patients.
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