目的 探讨miR-4505在先天性巨结肠（HSCR）中的作用及分子机制。 方法 选取HSCR病变段肠管及扩张段肠管组织标本，qRT-PCR检测组织标本miR-4505表达量；分别选用miR-4505模拟物及抑制剂转染人神经母细胞株SH-SY5Y，qRT-PCR检测转染后miR-4505表达，CCK-8及Transwell检测miR-4505对细胞增殖及细胞迁移的影响；生物信息学预测、双荧光素酶报告基因实验、Western blot以及免疫组织化学在细胞及组织层面证实SOX-10是miR-4505的作用靶点。 结果 与扩张段肠管相比，HSCR病变段肠管的miR-4505呈高频高表达（t = 11.25，P < 0.001）；过表达miR-4505可以抑制细胞增殖及迁移，敲低其表达后细胞的增殖及迁移能力增强；靶基因预测及双荧光素酶报告基因检测证实miR-4505可与SOX-10的3′-UTR结合，Western blot证实其可降低细胞SOX-10蛋白含量，而免疫组化证实SOX-10在HSCR病变段肠管中呈低表达。 结论 miR-4505在HSCR病变段及扩张段肠管之间存在表达差异，miR-4505可以抑制细胞的增殖及迁移，其在HSCR中发挥作用可能与抑制SOX-10基因表达有关。

Objective To explore the role and molecular mechanism of miR-4505 in Hirschsprung disease（HSCR）. Methods Stenotic and dilated colon segments of HSCR patients operated at Zhujiang Hospital of Southern Medical University were collected.qRT-PCR was performed to detected the expression of miR-4505 in colon tissuesspecimens.The miR-NC，miR-4505 mimics and miR-4505 inhibitors were transfected into human neuroblastoma cell line SH-SY5Y，followed by qRT-PCR to examine the expression of miR-4505 after transfection， CCK-8 assay and Transwell assay to detect the effect of miR-4505 on the proliferation and migration of SH-SY5Y cells.The downstream target genes of miR-4505 were predicted through bioinformatics and detected by dual luciferase reporter gene assay； the target genes were verified by Western blot and Immunohistochemistry. Results miR-4505 was highly expressed in the stenotic colon compared to the dilated segment （t = 11.25，P < 0.001）. Overexpression of miR-4505 inhibited cell proliferation and migration， and conversely，downregulation of miR-4505 enhanced cell proliferation and migration. Target gene prediction and dual-luciferase reporter gene assay suggested that the 3′-UTR of SOX-10 was a direct target of miR-4505. Moreover， Western blot confirmed that miR-4505 decreased SOX-10 protein levels in cells， while immunohistochemistry proved that SOX-10 was lowly expressed in HSCR disease colontissues. Conclusion Our study demonstrated that miR-4505 was differentially expressed between the diseased and dilated segments of HSCR.miR-4505 could inhibited cell proliferation and migration，and its role in HSCR may be achieved by suppressing the downstream SOX-10 gene expression.