口腔癌大多数是由口腔粘膜表面鳞状细胞的恶性转化引起的。然而，CEACAM1和口腔癌之间的关系尚不清楚。从基因表达综合数据库（GEO）下载了GSE23558和GSE25099的数据。筛选出差异表达基因（DEGs），并进行了加权基因共表达网络分析（WGCNA）。构建和分析蛋白质相互作用（PPI）网络。进行基因本体论（GO）和基因组基因百科全书（KEGG）以及基因集富集分析（GSEA），基因表达热图，免疫浸润分析，比较毒物基因组数据库（CTD）。TargetScan筛选出调节中心DEGs的miRNAs。进行了西方印迹（WB）实验。鉴定出了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、上皮细胞发育等方面。KEGG分析显示它们主要富集在癌症通路、PI3K/Akt信号通路、TNF信号通路、NF-kappa B信号通路、TGF-beta信号通路等方面。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，而CEACAM1在口腔癌样本中低表达。CEACAM1、CEP55和MELK参与了肿瘤、炎症、坏死和增殖。西方印迹（WB）显示口腔癌样本中的CEACAM1低于正常样本，CEACAM1敲除后低于口腔癌样本。口腔癌中CEACAM1表达低，CEACAM1表达越低，预后越差。

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.