Open AccessDifferential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma
Author(s) -
Li Shicheng,
Sun Xiao,
Miao Shuncheng,
Liu Jia,
Jiao Wenjie
Publication year - 2017
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.12510
Subject(s) - kegg , lung cancer , gene , long non coding rna , medicine , gene expression , microarray analysis techniques , microarray , transcription factor , cancer research , rna , biology , bioinformatics , computational biology , genetics , oncology , transcriptome
Background Cigarette smoking is one of the greatest preventable risk factors for developing cancer, and most cases of lung squamous cell carcinoma (lung SCC) are associated with smoking. The pathogenesis mechanism of tumor progress is unclear. This study aimed to identify biomarkers in smoking‐related lung cancer, including protein‐coding gene, long noncoding RNA, and transcription factors. Methods We selected and obtained messenger RNA microarray datasets and clinical data from the Gene Expression Omnibus database to identify gene expression altered by cigarette smoking. Integrated bioinformatic analysis was used to clarify biological functions of the identified genes, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, the construction of a protein–protein interaction network, transcription factor, and statistical analyses. Subsequent quantitative real‐time PCR was utilized to verify these bioinformatic analyses. Results Five hundred and ninety‐eight differentially expressed genes and 21 long noncoding RNA were identified in smoking‐related lung SCC. GO and KEGG pathway analysis showed that identified genes were enriched in the cancer‐related functions and pathways. The protein–protein interaction network revealed seven hub genes identified in lung SCC. Several transcription factors and their binding sites were predicted. The results of real‐time quantitative PCR revealed that AURKA and BIRC5 were significantly upregulated and LINC00094 was downregulated in the tumor tissues of smoking patients. Further statistical analysis indicated that dysregulation of AURKA , BIRC5 , and LINC00094 indicated poor prognosis in lung SCC. Conclusion Protein‐coding genes AURKA , BIRC5 , and LINC00094 could be biomarkers or therapeutic targets for smoking‐related lung SCC.