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Genes involved in keratinization, keratinocyte and epithelium differentiation are aberrantly regulated in oral lichen planus
被引:0
|作者:
Qing Liu
Yuan Liu
Xinwen Wang
Jie Xu
Wei Zhou
机构:
[1] Fourth Military Medical University,Department of Periodontology and Oral Medicine, School of Stomatology
[2] Fourth Military Medical University,Department of Oral Pathology School of Stomatology
[3] The 309th Hospital of Chinese PLA,Department of Stomatology
来源:
关键词:
Oral lichen planus;
Differentially expressed genes;
Protein–protein interaction network;
Enrichment analysis;
Transcription factor binding sites;
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摘要:
Oral lichen planus (OLP) is a common inflammatory oral mucosal disease and a potential premalignant status of oral squamous cell carcinoma. This study aims to explore the molecular mechanisms of OLP. The gene expression dataset (GSE38616) of OLP tissues and healthy controls was downloaded from Gene Expression Omnibus database. After preprocessing the raw data through affy package, limma package was utilized to identify differentially expressed genes (DEGs) (criteria: p ≤ 0.05 and |log2 fold change| ≥ 2). Then, functional and pathway enrichment analyses were performed by using DAVID software (criterion: p value <0.1). Besides, STRING sever was utilized to investigate protein–protein interactions (PPIs) based on which PPI network was constructed (criterion: combined score >0.4). Finally, the transcription factor binding sites (TFBSs) of DEGs were predicted through WGRV software (criterion: p value <0.0001). A total of ten DEGs were identified, including two down-regulated and eight up-regulated DEGs, which were enriched in nine functions mainly about keratinization, differentiation and development of keratinocyte and epithelium. Besides, PPI network was constructed, and CXCL13 was a hub gene. Furthermore, four conserved TFBSs (AR, dlx3, ALX-3, and Msx-1) were co-existed in SLC6A14, CXCL13, and CDSN. CDSN, LCE3D, LCE3E, and SPRR2B might play a role in OLP through participating in keratinization, differentiation and development of keratinocyte and epithelium, while EIF1AY, WFDC12, and CXCL13 might participate in OLP through regulating inflammation and immunity. These predictions might promote the understanding of OLP mechanism. However, further studies are required to validate the bioinformatics outcomes.
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页码:751 / 757
页数:6
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