Abstract:
:Adenoid cystic carcinoma (ACC) is one of the most frequent malignancies of salivary glands. The objective of this study was to identify key genes and potential mechanisms during ACC samples.The gene expression profiles of GSE88804 data set were downloaded from Gene Expression Omnibus. The GSE88804 data set contained 22 samples, including 15 ACC samples and 7 normal salivary gland tissues. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were constructed, and protein-protein interaction network of differentially expressed genes (DEGs) was performed by Cytoscape. The top 10 hub genes were analyzed based on Gene Expression Profiling Interactive Analysis. Then, DEGs between ACC samples and normal salivary gland samples were analyzed by gene set enrichment analysis. Furthermore, miRTarBase and Cytoscape were used for visualization of miRNA-mRNA regulatory network. KEGG pathway analysis was undertaken using DIANA-miRPath v3.0.In total, 382 DEGs were identified, including 119 upregulated genes and 263 downregulated genes. GO analysis showed that DEGs were mainly enriched in extracellular matrix organization, extracellular matrix, and calcium ion binding. KEGG pathway analysis showed that DEGs were mainly enriched in p53 signaling pathway and salivary secretion. Expression analysis and survival analysis showed that ANLN, CCNB2, CDK1, CENPF, DTL, KIF11, and TOP2A are all highly expressed, which all may be related to poor overall survival. Predicted miRNAs of 7 hub DEGs mainly enriched in proteoglycans in cancer and pathways in cancer.This study indicated that identified DEGs and hub genes might promote our understanding of molecular mechanisms, which might be used as molecular targets or diagnostic biomarkers for ACC.
journal_name
Medicine (Baltimore)journal_title
Medicineauthors
Liu HB,Huang GJ,Luo MSdoi
10.1097/MD.0000000000018676subject
Has Abstractpub_date
2020-01-01 00:00:00pages
e18676issue
2eissn
0025-7974issn
1536-5964pii
00005792-202001100-00051journal_volume
99pub_type
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