钙结合蛋白S100A11促进结直肠癌进展的作用及其机制研究  

Role of calcium binding protein S100A11 promoting the progression of colorectal cancer and its mechanism

作　　者：宁俊娅 刘敏[1] 张姣姣 高丽娟 曹济民 NING Junya;LIU Min;ZHANG Jiaojiao;GAO Lijuan;CAO Jimin(Key Laboratory of Cell Physiology at Shanxi Medical University,Ministry of Education,Key Laboratory of Cell Physiology of Shanxi Province,and the Department of Physiology,Shanxi Medical University,Shanxi Taiyuan 030001,China)

机构地区：[1]山西医科大学细胞生理学教育部重点实验室,山西省细胞生理学重点实验室,山西医科大学生理学系,山西太原030001

出　　处：《现代肿瘤医学》2024年第3期405-411,共7页Journal of Modern Oncology

基　　金：国家自然科学基金项目(编号:82203412)。

摘　　要：目的:探讨钙结合蛋白S100A11调控结直肠癌(colorectal cancer,CRC)进展的作用及其机制。方法:利用GEPIA、UALCAN和HPA等数据库分析S100A11在CRC中的表达情况及其与CRC临床分期和预后的关系,并利用CRC细胞系/永生化肠上皮细胞进行验证,利用RNA干扰实验进一步分析S100A11对CRC细胞迁移及CRC生物学通路的影响。结果:数据库分析结果显示,与正常结直肠组织相比,S100A11在CRC组织中表达显著升高,并且S100A11与CRC的晚期分期及不良预后密切相关。RT-qPCR和Western blot结果也显示,S100A11在CRC细胞中表达升高。敲低S100A11能够有效抑制SW480细胞的迁移和上皮间质转化(epithelial-mesenchymal transition,EMT)过程。沉默CRC细胞中S100A11的表达后,利用转录组测序和生信分析,共筛选出149个差异表达基因,这些差异表达基因的功能网络富集结果主要涉及到炎症性肠病、黏着斑和PI3K-Akt信号通路等。结论:本研究发现高表达的S100A11是CRC转移的重要因素,并初步揭示S100A11调控CRC细胞的关键信号通路,为深入探讨S100A11调控CRC进展的分子机制提供了实验依据。Objective:To investigate the effect and mechanism of calcium binding protein S100A11 in regulating colorectal cancer(CRC)progression.Methods:In this study,GEPIA,UALCAN and HPA databases were used to analyze the expression of S100A11 in CRC and its relationship with the clinical stage and prognosis of CRC.In addition,CRC cell lines/immortalized intestinal epithelial cell were used for verification.The effect of S100A11 on CRC cell migration and CRC biological pathway was further analyzed by RNA interference assay.Results:Database analysis showed that the expression of S100A11 in CRC tissues was significantly higher than that in normal colorectal tissues.And S100A11 was closely associated with the late stage and poor prognosis of CRC.RT-qPCR and Western blot results also showed that the expression of S100A11 was increased in CRC cells.Knocking down S100A11 in SW480 cells effectively inhibited cell migration and epithelial-mesenchymal transition(EMT)process.After silencing S100A11 expression in CRC cells,a total of 149 differentially expressed genes were screened by transcriptome sequencing and biogenic analysis.The functional networks enrichment results of these differentially expressed genes were mainly involved in inflammatory bowel disease,focal adhesion and PI3K-Akt signaling pathway.Conclusion:This study found that high expression of S100A11 is an essential factor in CRC metastasis,and preliminarily revealed the key signaling pathways regulated by S100A11 in CRC cells,providing experimental basis for further exploration of the molecular mechanism by which S100A11 regulating CRC progression.

关 键 词：S100A11 结直肠癌 细胞迁移 生物信息学 基因表达调控 

分 类 号：R735.3[医药卫生—肿瘤]