Abstract
The mechanisms that underlie long non-coding RNA 00092 (LINC00092) in lung adenocarcinoma (LUAD) remain unclear. In this study, by mining the Cancer Genome Atlas and Gene Expression Omnibus databases and using bioinformatics tools, we try to elucidate the function of LINC00092 in LUAD.The the Cancer Genome Atlas and gene expression Omnibus microarray datasets were used to analyze and evaluate the expression of LINC00092 in LUAD and its clinical significance. Clinical samples were collected and the relative expression level of LINC00092 were identified by quantitative real time polymerase chain reaction. The LINC00092 related genes were identified by Multi Experiment Matrix, The Atlas of ncRNA in Cancer and the database of RNA-Binding Protein specificities. The predicted genes were then sent to the Gene Ontology enrichment and the Kyoto Encyclopedia of Genes and Genomes pathway analysis.The expression of LINC00092 was significantly decreased in LUAD tissues compared to non-tumor tissues (standard mean difference =-1.10, 95% confidence interval: -1.87 to -0.32, P < .001, random). Low expression of LINC00092 was associated with the poor overall survival (hazard ratio = 1.32, 95% confidence interval: 1.08-1.62, P < .05, fixed) and high pathological stage (P < .05). The relative expression level of LINC00092 in clinical samples were significantly lower in LUAD tissues compared with adjacent normal tissues. (P < 0.05) 61 LINC00092 related genes were identified; the Kyoto Encyclopedia of Genes and Genomes analysis showed that the most significant signaling pathways were: NF-κB, HIF-1 and ErbB signaling pathways.In this study, we found that the decrease of LINC00092 expression was involved in LUAD tumorigenesis and metastasis, and the depletion of LINC00092 was associated with a poor prognosis in patients with LUAD. The mechanisms that underlie LINC00092 in LUAD might be related to the NF-κB, HIF-1 and ErbB signaling pathways.