<b>DLEU2 facilitates bladder cancer progression through </b><b>miR-103a-2-5p/SOS1</b><b> axis</b>

<b>Background:</b> Bladder cancer (BC) is a life-threatening malignancy of the urinary system. Dysregulation of lncRNA acts vital role in various progression of BC. However, the function with potential regulation mechanism of lncRNA DLEU2 in BC cells remains no clue.<b>Methods:</b> The expression profiles of lncRNAs, miRNAs, along with mRNA in normal bladder tissues or BC tissues were analyzed by utilizing raw data obtained from NCBI GEO database. The lncRNAs, miRNAs, along with mRNA expression in BC cells were evaluated through application of RT-qPCR. CCK-8 along with Edu assay, Transwell along with scratch assay were assessed BC cells proliferation, migration, respectively. Luciferase experiment was exerted to inspect the interaction between DLEU2 with miRNAs (including miR-103a-2-5p), miR-103a-2-5p with SOS1. The SOS1 protein expression in BC cells was evaluated using western blot.<b>Results: </b>DLEU2 was the most differentially high expressed in BC. Functionally, DLEU2 overexpression could facilitate BC cells proliferation with migration, while DLEU2 knockdown had opposite effects. DLEU2 sponged miR-103a-2-5p. miR-103a-2-5p knockdown could facilitate BC cells proliferation with migration, while miR-103a-2-5p knockdown + DLEU2 knockdown had opposite effects. SOS1 was a target of miR-103a-2-5p. SOS1 overexpression could facilitate BC cells proliferation with migration, while SOS1 overexpression + miR-103a-2-5p overexpression had the opposite effects; SOS1 knockdown could block BC cells proliferation with migration, while SOS1 knockdown + miR-103a-2-5p knockdown had opposite effects.<b>Conclusions:</b> Our findings verified that DLEU2 facilitates BC progression through miR-103a-2-5p/SOS1 axis.

**背景：** 膀胱癌（Bladder cancer, BC）是一类危及生命的泌尿系统恶性肿瘤。长链非编码RNA（long non-coding RNA, lncRNA）的失调在膀胱癌的多种病程进展中发挥关键调控作用，但长链非编码RNA DLEU2在膀胱癌细胞中的功能及潜在调控机制仍不明确。**方法：** 本研究利用美国国家生物技术信息中心基因表达综合数据库（NCBI GEO）的原始数据，分析正常膀胱组织与膀胱癌组织中lncRNA、微小RNA（microRNA, miRNA）及信使RNA（messenger RNA, mRNA）的表达谱；采用实时荧光定量聚合酶链反应（RT-qPCR）检测膀胱癌细胞中lncRNA、miRNA及mRNA的表达水平；分别通过细胞计数试剂盒-8（CCK-8）、5-乙炔基-2'-脱氧尿苷增殖实验（Edu assay）、Transwell实验及划痕实验评估膀胱癌细胞的增殖、迁移能力；采用双荧光素酶报告基因实验验证DLEU2与miR-103a-2-5p、miR-103a-2-5p与SOS1之间的相互作用；采用蛋白质印迹法（western blot）检测膀胱癌细胞中SOS1蛋白的表达水平。**结果：** DLEU2在膀胱癌组织中呈显著高表达。功能实验显示，过表达DLEU2可促进膀胱癌细胞的增殖与迁移，而敲低DLEU2则产生相反效应。DLEU2可作为分子海绵吸附miR-103a-2-5p。敲低miR-103a-2-5p可促进膀胱癌细胞的增殖与迁移，而同时敲低DLEU2与miR-103a-2-5p则可逆转该促进作用。SOS1是miR-103a-2-5p的靶基因。过表达SOS1可促进膀胱癌细胞的增殖与迁移，而同时过表达SOS1与miR-103a-2-5p则可抵消该促进效应；敲低SOS1可抑制膀胱癌细胞的增殖与迁移，而同时敲低SOS1与miR-103a-2-5p则可逆转该抑制作用。**结论：** 本研究证实，DLEU2通过调控miR-103a-2-5p/SOS1轴促进膀胱癌的进展。