3201 Hospital, Han Zhong, Shaanxi, China.
Medicine (Baltimore). 2024 Sep 6;103(36):e39408. doi: 10.1097/MD.0000000000039408.
Colorectal adenocarcinoma (COAD) has a poor prognosis. Cyclin-dependent kinase inhibitor 2A (CDKN2A) significantly affects the development and progression of various human tumors. However, the significance and pathological mechanisms of CDKN2A in COAD remain to be elucidated. We assessed expression levels, clinical significance, biological function, co-expressed genes, and enrichment of related pathways of CDKN2A in COAD using various databases, including The University of Alabama at Birmingham Cancer Data Analysis Portal, Gene Expression Profiling Interactive Analysis, Tumor Immune Estimation Resource, Human Protein Atlas, STRING, GeneMANIA, cBioPortal, and Linked Omics. Our investigation showed that CDKN2A was highly expressed in colon adenocarcinomas (P < .001). It is weakly expressed or not expressed in normal tissues. The survival time of patients with colon adenocarcinoma with high CDKN2A expression is significantly shorter than that of patients with low expression levels (P = .011). There was a significant positive correlation between the expression level of CDKN2A in colon adenocarcinoma tissues and the infiltration of CD4+ T cells, macrophages, and neutrophils. Moreover, there was a significant negative association between the expression level of CDKN2A in colon adenocarcinoma tissues and B cell infiltration. The ten hub genes included tumor protein 53, V-myc Avian Myelocytomatosis Viral Oncogene Homolog, AKT serine/threonine kinase 1, cyclin-dependent kinase 2, phosphatase and tensin homolog deleted on chromosome ten, cyclin D1, cyclin dependent kinase 4, cyclin dependent kinase inhibitor 1A, catenin beta 1, and B-Raf proto-oncogene, serine/threonine kinase. Mutations in the CDKN2A genome in colon adenocarcinoma reduce survival. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed that the differentially expressed genes were enriched in apoptotic signaling pathways and multiple pathways related to metabolic progression. Our results indicate that CDKN2A can be used as a marker of poor prognosis in patients with colon adenocarcinoma. CDKN2A may regulate the occurrence and development of colon adenocarcinomas by influencing immune cell infiltration and metabolic pathways.
结直肠癌（COAD）预后不良。细胞周期蛋白依赖性激酶抑制剂 2A（CDKN2A）显著影响各种人类肿瘤的发生和发展。然而，CDKN2A 在 COAD 中的意义和病理机制仍有待阐明。我们使用包括阿拉巴马大学伯明翰癌症数据分析门户、基因表达谱交互式分析、肿瘤免疫估计资源、人类蛋白质图谱、STRING、GeneMANIA、cBioPortal 和链接组学在内的各种数据库评估了 CDKN2A 在 COAD 中的表达水平、临床意义、生物学功能、共表达基因和相关途径的富集情况。我们的研究表明，CDKN2A 在结肠腺癌中高表达（P <.001）。在正常组织中弱表达或不表达。CDKN2A 高表达的结肠腺癌患者的生存时间明显短于低表达水平的患者（P =.011）。结肠腺癌组织中 CDKN2A 的表达水平与 CD4+T 细胞、巨噬细胞和中性粒细胞的浸润呈显著正相关。此外，结肠腺癌组织中 CDKN2A 的表达水平与 B 细胞浸润呈显著负相关。十个枢纽基因包括肿瘤蛋白 53、V-myc 禽髓细胞瘤病毒致癌基因同源物、AKT 丝氨酸/苏氨酸激酶 1、细胞周期蛋白依赖性激酶 2、染色体 10 缺失的磷酸酶和张力蛋白同源物、细胞周期蛋白 D1、细胞周期蛋白依赖性激酶 4、细胞周期蛋白依赖性激酶抑制剂 1A、连环蛋白 β 1 和 B-Raf 原癌基因丝氨酸/苏氨酸激酶。结肠腺癌中 CDKN2A 基因组的突变降低了生存率。基因本体论和京都基因与基因组百科全书分析表明，差异表达基因富集在凋亡信号通路和与代谢进展相关的多个途径中。我们的结果表明，CDKN2A 可作为结肠腺癌患者预后不良的标志物。CDKN2A 可能通过影响免疫细胞浸润和代谢途径来调节结肠腺癌的发生和发展。
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