结直肠癌中SAA2表达与肿瘤免疫微环境的关系

Expression of SAA2 in colorectal cancer and its association with tumor immune microenvironment

目的:探究血清淀粉样蛋白2(SAA2)在结直肠癌中的表达及与肿瘤免疫浸润微环境的关系。方法:生物信息学和Western blot分析SAA2在结直肠癌中的表达水平;Log-rank法分析SAA2表达对总生存期的影响;CIBERSORT法分析肿瘤纯度得分、免疫得分及肿瘤组织中基质得分与SAA2表达的相关性;TISIDB分析SAA2与CD274等免疫分子的相关性;聚类分析鉴定结直肠癌中SAA2相关的信号通路。结果:SAA2在结直肠癌肿瘤组织中基因和蛋白均高表达;SAA2高表达的结直肠癌患者总生存期显著低于SAA2低表达组;结直肠癌肿瘤组织中SAA2表达水平与肿瘤组织中肿瘤细胞纯度和肿瘤免疫得分呈正相关,而与基质得分无显著相关性;SAA2与CD274等免疫抑制性分子呈正相关,而与趋化因子、细胞因子受体相互作用、自然杀伤细胞介导的细胞毒作用、抗原呈递等信号通路呈负相关。结论:结直肠癌肿瘤细胞中SAA2呈高表达,其高表达提示结直肠癌患者的不良预后,且SAA2高表达与免疫抑制微环境存在紧密联系。

Objective:To explore the expression of serum amyloid A2(SAA2)in colorectal cancer and its association with tumor immune infiltration microenvironment.Methods:Bioinformatics and Western blot were used to analyze expression of SAA2 in colorectal tumor.Effect of SAA expression on overall survival was conducted by Log-rank method.CIBERSORT method was subjected to explain the correlation between SAA2 expression and tumor purity score,immune score and tumor stromal score.Correlations analysis between SAA2 and CD274 and other mediators were achieved by TISIDB database.Gene enrichment analysis identified SAA2-related signaling pathways.Results:SAA2 was highly expressed in colorectal cancer in both gene and protein levels.Survival time of SAA2high expression group was lower than SAA2 low expression group.SAA2 expression level was positively correlated with tumor purity and tumor immune score in colorectal cancer,but there was no significant correlation with tumor stromal score.SAA2 was positively correlated with CD274 and other tumor immune-suppression molecules,but negatively correlated with chemokine signaling pathway,cytokine-cytokine receptor interaction,natural killer cell mediated cytotoxicity and antigen processing and presentation in colorectal cancer.Conclusion:SAA2 is high expression in colorectal cancer,the higher expression predicts poor prognosis of colorectal cancer patients,and the higher expression of SAA2 is also closely associated with tumor immune-suppression microenvironment.