Department of Stomatology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075000, China.
Department of Central Sterile Supply, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075000, China.
Aging (Albany NY). 2023 Aug 16;15(16):8137-8154. doi: 10.18632/aging.204960.
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.
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.
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.
CEACAM1 is lowly expressed in oral cancer, the lower CEACAM1, the worse prognosis.
大多数口腔癌是由口腔黏膜表面鳞状细胞的恶性转化引起的。然而，CEACAM1 与口腔癌之间的关系尚不清楚。
从基因表达综合数据库（GEO）下载 GSE23558 和 GSE25099 谱。筛选差异表达基因（DEGs）并进行加权基因共表达网络分析（WGCNA）。构建和分析蛋白质-蛋白质相互作用（PPI）网络。进行基因本体论（GO）和京都基因与基因组百科全书（KEGG）、基因集富集分析（GSEA）、基因表达热图、免疫浸润分析、比较毒理学基因组数据库（CTD）。TargetScan 筛选调节核心 DEGs 的 miRNAs。进行 Western blot（WB）实验。
鉴定出 1269 个 DEGs。根据 GO 分析，它们主要富集在相同的蛋白质结合、信号受体结合、细胞表面、上皮细胞发育中。KEGG 分析表明，它们主要富集在癌症途径、PI3K Akt 信号通路、TNF 信号通路、NF-κB 信号通路、TGF-β信号通路中。PPI 网络显示获得了 11 个基因（CDCA8、CCNA2、MELK、KIF2C、CDC45、HMMR、TPX2、CENPF、CDK1、CEP55、CEACAM1）。基因表达热图显示 CEP55 和 MELK 在口腔癌样本中高表达。CEACAM1 在口腔癌样本中低表达。CEACAM1、CEP55 和 MELK 参与肿瘤、炎症、坏死和增殖。Western blot（WB）显示口腔癌样本中的 CEACAM1 低于正常样本，CEACAM1 敲低后，低于口腔癌样本。
CEACAM1 在口腔癌中低表达，CEACAM1 越低，预后越差。
