子宫内膜细胞如何接收内外信号引起细胞迁徙是EMs发病及复发的关键步骤，本项目利用前期lnc芯片筛查出在异位子宫内膜细胞显著高表达的lncRNA-uc010fhn.2，并通过mRNA共表达分析筛选出受其正调控且与肿瘤细胞迁徙密切相关的共表达基因CTHRC1，探讨lncRNA-uc010fhn.2介导CTHRC1调控异位子宫内膜细胞迁徙的作用及机制。项目通过正向激活、反向抑制lncRNA-uc010fhn.2的方法转染子宫内膜细胞，运用transwell实验、激光扫描共聚焦等手段，揭示lncRNA-uc010fhn.2与子宫内膜细胞迁徙的相关性；采用免疫共沉淀技术确定与CTHRC1相互作用、可能参与子宫内膜细胞迁徙的候选信号蛋白和传导通路，检测沉默后CTHRC1及候选信号分子的表达变化，并进行体内验证。本项目从新的角度深入揭示EMs的发病机制，有望为内异症的早期诊断、治疗及预后提供新的策略。

How endometrial cell receive celluar signals to migrate outside is the key step in the process of EMs incidence and recurrence. The present research take advantage of our previous lncRNA chip research results, that highly expressed lncRNA-uc010fhn.2 and its closely related gene CTHRC1 to explore how lncRNA-uc010fhn.2 induce CTHRC1 to regulate endometrial cell migration. After forward activation and reverse inhibition of lncRNA-uc010fhn.2 in endometrial cell, transwell experiment and confocal laser scanning microscopy methods are used to reveal the relationship of lncRNA-uc010fhn.2 and endometrial cell migration. Then immune co-precipitation technique is applied to define the candidate signal proteins and pathways, which directly interact with CTHRC1 and related to endometrial cell migration. Furthermore, we detect the candidate signal molecules expression changes by realtime RT-PCR and westernblot analysis. In the end, we testify all the invitro effects through invivo test. This project intends to further explore the pathogenesis of EMs from a new angle of view. We hope it will help to provide some new targets for the early diagnosis, treatment and prognosis of endometriosis.