基于生物信息学筛选炎症相关结直肠癌基因及其特征分析

Screening and characterization of inflammation-related genes in colorectal cancer based on bioinformatics

目的通过对炎症性肠病差异基因的筛选以及结直肠癌队列生存特征和表达模式的探究,为炎症相关结直肠癌的发生与发展的后续研究提供候选基因。方法从GEO数据库中选择RNA测序表达谱数据集GSE95473和GSE107597,通过常规转录组表达谱差异分析,筛选出炎症性肠病差异表达基因(DEG),利用GO数据库获取DEG的功能注释,并利用KEGG数据库进行通路富集分析。同时基于TCGA数据库进一步在结直肠癌数据集中筛选具有预后意义的基因,并评价其在结直肠肿瘤中的表达特征。结果两个数据集筛选到了共有DEGs 100个,通过主成分分析证实这些基因能够对结直肠癌肿瘤和黏膜区分良好。进一步筛选,获得ALDOB,SPINK4,REG4,IL1B,C2CD4A,CXCL8,NOS2,CXCL3等候选基因。这些基因在结直肠肿瘤中高表达,并且这些基因的高表达往往提示患者预后较好。结论ALDOB,SPINK4,REG4,IL1B,C2CD4A,CXCL8,NOS2,CXCL3可能在炎症相关结直肠癌的发生发展中发挥重要作用,有待于后续炎癌转化相关功能验证和机制探究。

Objective To explore the differential characteristics of inflammatory bowel disease and the survival characteristics and expression patterns of colorectal cancer cohort.Further,candidate genes are provided for subsequent studies on the development of inflammation-related colorectal cancer.Methods The RNA sequencing expression profile data sets GSE95473 and GSE107597 were selected from the GEO database.The inflammatory bowel disease expression differential gene(DEG)was screened by routine transcriptome expression profiling analysis.The GO database and the KEGG database were used to obtain functional annotations of the DEG and path enrichment analysis respectively.At the same time,based on the TCGA database,the prognostic genes were further screened in the colorectal cancer dataset,and their expression characteristics in colorectal tumors were evaluated.Results Two datasets were screened for 100 common DEGs,which were confirmed by principal component analysis to distinguish well between colorectal cancer tumors and mucosa.Further screening,candidate genes such as ALDOB,SPINK4,REG4,IL1B,C2CD4A,CXCL8,NOS2,CXCL3 were obtained.These genes are highly expressed in colorectal tumors,and high expression of these genes often suggests a better prognosis.Conclusion ALDOB,SPINK4,REG4,IL1B,C2CD4A,CXCL8,NOS2,CXCL3 may play an important role in the development of inflammation-related colorectal cancer,and it is necessary to verify the function and mechanism of subsequent inflammation transformation.