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CEACAM1 as a molecular target in oral cancer
Sai Ma1, Zhonghua Wang1, Chao Li1
1Department of Stomatology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075000, China.
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.
Insights
Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is significantly downregulated in oral cancer, correlating with poorer patient prognosis. This suggests CEACAM1 may serve as a potential biomarker for oral squamous cell carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Oral cancer, primarily squamous cell carcinoma, arises from oral mucosa transformation.
- The role of Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in oral cancer pathogenesis remains largely undefined.
Purpose of the Study:
- To investigate the expression profile and potential role of CEACAM1 in oral cancer.
- To identify key molecular pathways and genes associated with oral cancer development.
Main Methods:
- Analysis of gene expression datasets (GSE23558, GSE25099) to identify differentially expressed genes (DEGs).
- Weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) network construction.
- Gene Ontology (GO), Kyoto Encyclopedia of Gene and Genome (KEGG), and Western blotting (WB) analyses were performed.
Main Results:
- 1269 DEGs were identified, enriched in cancer-related pathways like PI3K-Akt and TGF-beta signaling.
- CEACAM1 was identified as a key gene in the PPI network and was found to be significantly downregulated in oral cancer tissues.
- Western blotting confirmed lower CEACAM1 expression in oral cancer samples, with further reduction upon CEACAM1 knockdown.
Conclusions:
- CEACAM1 exhibits low expression in oral cancer, indicating a potential inverse correlation with disease progression.
- Reduced CEACAM1 levels are associated with a worse prognosis in oral cancer patients, highlighting its potential as a prognostic biomarker.
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