首页|miR-3917通过调控Wnt/β-catenin信号通路抑制结肠癌细胞的增殖和迁移

miR-3917通过调控Wnt/β-catenin信号通路抑制结肠癌细胞的增殖和迁移

miR-3917 inhibits the proliferation and migration of colorectal cancer cells by regulating the Wnt/β-catenin signaling path-way

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目的 探究miR-3917在结肠癌(Colorectal cancer,CRC)细胞增殖和迁移中的作用及相关信号通路机制.方法 应用GEO2R分析工具对miRNA表达数据集(GSE101502)进行比较分析,获取在CRC组织中差异表达的miRNA.在TCGA数据库的样本表达数据中验证目的miRNA的表达水平.进一步通过qPCR检测miR-3917在人正常结肠细胞系(CCD841 CoN)和CRC细胞系(HCT 116)中的表达水平.通过在HCT 116细胞中转染miR-3917的模拟物(miR-mimic)上调其表达,并利用qPCR检测验证.通过CCK-8实验和平板克隆形成实验检测细胞的增殖.通过划痕实验和Transwell迁移实验检测细胞的迁移.通过TargetScan对miR-3917的靶基因进行预测并利用DA-VID数据库对其进行富集分析.通过Western blot检测β-catenin核蛋白的表达以评价Wnt/β-catenin信号通路的激活水平.结果 共有21个差异表达的miRNA(Log2 | Fold Change |>1,P<0.05),其中与正常组织相比较,CRC组织中上调的有2个,下调的有19个.miR-3917在CRC组织中的表达显著下降(P<0.05).与CCD841 CoN细胞系相比,HCT 116细胞中miR-3917的表达显著降低(P<0.05).在HCT 116细胞中转染miR-mimic可以显著上调miR-3917的表达(P<0.05).与对照组相比,miR-mimic组中HCT 116细胞的增殖(CCK-8实验,P<0.05;平板克隆形成实验,P<0.05)和迁移(划痕实验,P<0.05;Transwell实验,P<0.05)能力显著下降.与对照组相比,miR-mimic组中HCT 116细胞Wnt/β-catenin信号通路被显著抑制(P<0.05).结论 miR-3917通过调控Wnt/β-catenin信号通路抑制CRC细胞的增殖和迁移能力,这为CRC的治疗提供了潜在新靶点.
Objective To investigate the role of miR-3917 in the proliferation and migration of colorectal cancer(CRC)cells and associated signaling pathway mechanism.Methods GEO2R tool was used to analyze the miRNA ex-pression dataset(GSE101502)to obtain differentially expressed miRNAs in CRC tissues.The expression level of target miRNA was verified in the sample expression data from TCGA database.The expression levels of miR-3917 in human normal colon cell line(CCD841 CoN)and CRC cell line(HCT 116)were detected by qPCR.The expression of miR-3917 was up-regulated by transfecting its mimic in HCT 116 cells,and the expression was verified by qPCR.The cell prolif-eration was assessed by CCK-8 assay and plate colony formation assay.The cell migration was assessed by wound-heal-ing assay and Transwell migration assay.The target genes of miR-3917 were predicted using TargetScan,and enrich-ment analysis was performed with DAVID database.The expression of nuclear β-catenin protein was detected by West-ern blot to evaluate the activation level of Wnt/β-catenin signaling pathway.Results A total of 21 differentially ex-pressed miRNAs(Log2 | Fold Change |>1,P<0.05)were identified,of which 2 were up-regulated and 19 were down-regulated in CRC tissues compared to normal tissues.The expression of miR-3917 significantly decreased in CRC tissues(P<0.05).Compared with the CCD841 CoN cell line,the expression of miR-3917 in HCT 116 cell line signifi-cantly decreased(P<0.05).Transfecting miR-mimic in HCT 116 cells could significantly up-regulate the expression of miR-3917(P<0.05).The proliferation(CCK-8 assay,P<0.05;plate colony formation assay,P<0.05)and migration(wound-healing assay,P<0.05;Transwell assay,P<0.05)abilities of HCT 116 cells in the miR-mimic group signifi-cantly decreased compared with those in the control group.The Wnt/β-catenin signaling pathway of HCT 116 cells in the miR-mimic group was significantly inhibited(P<0.05)compared with that in the control group.Conclusion miR-3917 inhibits the proliferation and migration of CRC cells by regulating the Wnt/β-catenin signaling pathway,which provides a potential new target for the treatment of CRC.

miR-3917Wnt/β-catenin signaling pathwaycolorectal cancercell proliferationcell migration

吴坤、姜洋

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吉林大学中日联谊医院胃肠结直肠肛门外科,吉林长春 130033

miR-3917 Wnt/β-catenin信号通路 结肠癌 细胞增殖 细胞迁移

2024

中国实验诊断学
吉林大学中日联谊医院 上海交通大学医学院附属瑞金医院

中国实验诊断学

CSTPCD
影响因子:1.273
ISSN:1007-4287
年,卷(期):2024.28(1)
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