武汉市第一医院泌尿外科;
目的 探讨长链非编码RNA表面活性剂相关1假基因(SFTA1P)通过调控微小RNA-182-5p(miR-182-5p)/纤连蛋白1(FN1)通路促进肾透明细胞癌(ccRCC)细胞增殖与迁移的分子机制。方法 应用GEPIA2软件探究TCGA数据库中SFTA1P在ccRCC组织中的表达；实时定量PCR(qPCR)检测SFTA1P在ccRCC组织、正常肾脏组织及ccRCC细胞系中的表达；亚细胞定位实验探究SFTA1P在ccRCC细胞系人肾细胞腺癌细胞(ACHN)中的定位；将ACHN细胞分为si-Con组、si-SFTA1P#2组、mimic NC组、miR-182-5p mimic组、anti-miR-Con组、anti-miR-182-5p组、anti-miR-182-5p+si-FN1组、si-Con+anti-miR-Con组、si-SFTA1P#2+anti-miR-Con组及si-SFTA1P#2+anti-miR-182-5p组；CCK-8与transwell小室实验检测细胞增殖与迁移能力；qPCR、Western blot和双荧光素酶报告基因实验检测SFTA1P、miR-182-5p和FN1的调控关系。结果 TCGA数据库分析显示，SFTA1P在ccRCC组织中高表达(P<0.05);与正常肾脏组织比较，SFTA1P在ccRCC组织中表达升高(P<0.01);ccRCC细胞系786-O、SN12-PM6、ACHN及A498中SFTA1P表达明显高于人肾近曲小管细胞HK-2(均P<0.01);亚细胞定位实验显示SFTA1P主要分布于ACHN细胞的细胞质中；与si-Con组比较，si-SFTA1P#2组ACHN细胞增殖与迁移能力降低，FN1 mRNA及蛋白表达降低(P<0.05);与mimic NC组比较，miR-182-5p mimic组ACHN细胞FN1 mRNA及蛋白表达降低(P<0.01);与anti-miR-Con组比较，anti-miR-182-5p组ACHN细胞FN1 mRNA及蛋白表达增加，细胞增殖与迁移能力增强(P<0.05);与anti-miR-182-5p组相比，anti-miR-182-5p+si-FN1组ACHN细胞增殖与迁移能力降低(P<0.05);与si-SFTA1P#2+anti-miR-Con组比较，si-SFTA1P#2+anti-miR-182-5p组ACHN细胞增殖与迁移能力增强，FN1 mRNA及蛋白表达增加(P<0.05)。结论 SFTA1P在ccRCC中高表达，其通过调控miR-182-5p/FN1通路促进ccRCC细胞的增殖与迁移。
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基本信息:
DOI：10.19405/j.cnki.issn1000-1492.2025.01.006
中图分类号:R737.11
引用信息:
[1]向威,吕磊,郑福鑫等.LncRNA SFTA1P通过调控miR-182-5p/FN1通路促进肾透明细胞癌细胞增殖与迁移[J].安徽医科大学学报,2025,60(01):41-48.DOI:10.19405/j.cnki.issn1000-1492.2025.01.006.
基金信息:
国家自然科学基金(编号：81502204); 湖北省卫生健康委员会科研项目(编号：WJ2021Q001)~~