Abstract
This study was designed to explore the effects of tobacco smoke on gene expression through bioinformatics analyses. Gene expression profile GSE17913 was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in buccal mucosa tissues between 39 active smokers and 40 never smokers were identified. Gene Ontology (GO) and pathway enrichment analyses of DEGs were performed, followed by protein-protein interaction (PPI) network, transcriptional regulatory network as well as miRNA-target regulatory network construction. In total, 88 up-regulated DEGs and 106 down-regulated DEGs were identified. Among these DEGs, cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) and CYP1B1 were enriched in the Metabolism of xenobiotics by cytochrome P450 pathway. In the PPI network, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta (YWHAZ), and CYP1A1 were hub genes. In the transcriptional regulatory network, transcription factors of MYC associated factor X (MAX) and upstream transcription factor 1 (USF1) regulated many overlapped DEGs. In addition, protein tyrosine phosphatase, receptor type, D (PTPRD) was regulated by multiple miRNAs in the miRNA-DEG regulatory network. CYP1A1, CYP1B1, YWHAZ and PTPRD, and TF of MAX and USF1 may have the potential to be used as biomarkers and therapeutic targets in tobacco smoke-related pathological changes.
Highlights
There are approximately 1.3 billion people who smoke cigarettes in the world
The Metabolism of xenobiotics by cytochrome P450 pathway was enriched by several differentially expressed genes (DEGs) including cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) and CYP1B1
288 up-regulated DEGs and 106 down-regulated DEGs were identified. Among these DEGs, CYP1A1 and CYP1B1 were mainly enriched in the pathway of Metabolism of xenobiotics by cytochrome P450
Summary
There are approximately 1.3 billion people who smoke cigarettes in the world. Tobacco is an important risk factor for multiple human malignancies, which causes almost 5 million preventable deaths every year [1, 2]. More than 100 tumor promoters and carcinogens have been identified in tobacco [3]. Tobacco combustion products contain polycyclic aromatic hydrocarbons (PAHs), which have been suggested to be carcinogenic [4]. A variety of cancers such as lung cancer, oral cavity cancer, esophageal cancer and liver cancer are attributed to cigarette smoke [5]. Smoking can reduce the efficacy of targeted anticancer therapies by stimulating
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