Lung squamous cell carcinoma (LUSC), a type of non-small cell lung carcinoma, has a poor therapeutic response, high relapse rate and poor prognosis. The present study was designed to reveal the key long non-coding RNAs (lncRNAs) associated with the prognosis of LUSC. The lncRNA expression profiles of LUSC and adjacent samples were downloaded from The Cancer Genome Atlas database. Based on the edgeR and DEseq packages, the differentially expressed lncRNAs (DELs) between LUSC and adjacent samples were obtained and the intersecting DELs were regarded as significant DELs. Subsequently, a prognostic risk model was established using Cox regression analysis and its classification effect was detected by survival analysis. Using survival analysis, the effect of the prognostic risk model was assessed in the validation set and other types of cancer. Finally, the co-expression genes of key lncRNAs were screened using the Multi-Experiment Matrix tool and the STRING database, and their functions were predicted via enrichment analysis using the Database for Annotation, Visualization and Integrated Discovery tool. A total of 2,041 significant DELs between LUSC and adjacent samples were screened. The prognostic risk model consisting of RP5-821D11.7, APCDD1L-AS1 and RP11-277P12.9 was established, which had a good classification effect. Cox multivariate regression analysis demonstrated that risk score may serve as an independent prognostic factor. Furthermore, certain co-expression genes of RP5-821D11.7 (including proliferating cell nuclear antigen), APCDD1L-AS1 (including semaphorin 5A, semaphorin 6D, ADAMTS like 1, ADAM metallopeptidase with thrombospondin type 1 motif 6, slit guidance ligand 3, and tenascin C) and RP11-277P12.9 (including Wnt family member 2B) were identified. Additionally, ‘positive regulation of cell migration’ and ‘proteinaceous extracellular matrix’ were enriched. In conclusion, the expression levels of the lncRNAs RP5-821D11.7, APCDD1L-AS1 and RP11-277P12.9 may affect the prognosis of LUSC.
Targeted therapies based on EGFR mutations or on the ALK fusion oncogene have become the standard treatment for certain patients with lung adenocarcinoma (LUAD). However, most LUAD patients have no EGFR mutation or ALK fusion, and their oncogenetic alterations remain to be characterized. Here we conducted an integrated analysis of public datasets to assess the genomic alterations of 23 highly lung cancer-associated genes. The copy numbers of these genes were measured in ten micro-dissected, paired tumors and normal lung tissues of LUAD patients without EGFR mutations or ALK fusion. The copy numbers of PTEN, RB1, HMGA2, and PTPRD were lower in tumors compared with those for normal tissues. Although there were reduced mRNA levels of PTEN and RB1 in tumors, there was a correlation between copy number and expression only for PTEN. In addition, analysis of the copy number alterations of these 23 genes revealed correlations between EMSY/CCND1, EMSY/PIK3CA, CCND1/CDKN2A, and CCND1/PIK3CA. Our exploration of integrated copy number and gene expression analysis gives priority to the PTEN-PIK3CA and RB1-CCND1 pathways in developing therapeutic strategies for LUAD patients without EGFR mutations or ALK fusion.
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