Research Paper Volume 15, Issue 16 pp 8137—8154
CEACAM1 as a molecular target in oral cancer
- 1 Department of Stomatology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075000, China
- 2 Department of Central Sterile Supply, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075000, China
Received: May 15, 2023 Accepted: July 24, 2023 Published: August 16, 2023
https://doi.org/10.18632/aging.204960How to Cite
Copyright: © 2023 Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Objective: The majority of oral cancer is caused by malignant transformation of squamous cells in surface of the oral mucosa. However, the relationship between CEACAM1 and oral cancer is unclear.
Methods: GSE23558 and GSE25099 profiles were downloaded from gene expression omnibus (GEO). Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. Construction and analysis of protein-protein interaction (PPI) Network. Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG), gene set enrichment analysis (GSEA), gene expression heatmap, immune infiltration analysis, comparative toxicogenomics database (CTD) were performed. TargetScan screened miRNAs that regulated central DEGs. Western blotting (WB) experiment was performed.
Results: 1269 DEGs were identified. According to GO analysis, they were mainly enriched in same protein binding, signal receptor binding, cell surface, epithelial cell development. KEGG analysis showed that they were mainly enriched in cancer pathways, PI3K Akt signaling pathway, TNF signaling pathway, NF kappa B signaling pathway, TGF beta signaling pathway. PPI network showed that 11 genes (CDCA8, CCNA2, MELK, KIF2C, CDC45, HMMR, TPX2, CENPF, CDK1, CEP55, CEACAM1) were obtained. Gene expression heatmap showed that CEP55 and MELK were highly expressed in oral cancer samples. CEACAM1 was lowly expressed in oral cancer samples. CEACAM1, CEP55 and MELK were involved in tumor, inflammation, necrosis, and proliferation. Western blotting (WB) showed that CEACAM1 in oral cancer samples was lower than that in normal samples, after CEACAM1 knockdown, it was lower than that in oral cancer samples.
Conclusion: CEACAM1 is lowly expressed in oral cancer, the lower CEACAM1, the worse prognosis.
Abbreviations
GEO: gene expression omnibus; DEGs: differentially expressed genes; WGCNA: weighted gene co-expression network analysis; PPI: protein-protein interaction; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Gene and Genome; GSEA: gene set enrichment analysis; CTD: comparative toxicogenomics database; WB: western blotting; FC: fold change; FDR: false discovery rate; STRING: Search Tool for the Retrieval of Interacting Genes; KEGG: Kyoto Encyclopedia of Gene and Genome; CEA: Carcinoembryonic Antigen.