骨髓间充质干细胞（BMSCs）黏附造血细胞的能力低下是慢性粒细胞白血病(CML)进展及移植治疗失败的重要原因，但黏附缺陷具体机制未明。我们前期发现CML细胞外泌体携带高浓度miR-711，生物信息学分析显示其靶基因包括CD44、CXCL12、CCR9、CDH5等黏附相关分子。据此，我们提出"CML细胞通过外泌体携带转运miR-711抑制BMSCs黏附功能"的假说。我们拟通过激光共聚焦显微镜检查、细胞黏附实验、非接触共培养及动物模型共移植等体内外实验证实CML通过释放外泌体抑制BMSCs黏附功能；通过荧光素酶实验、过表达及抑制实验、RT-PCR及蛋白印迹等分子生物学实验证实外泌体的抑制作用是通过其携带的miR-711下调BMSCs黏附相关分子表达而实现的。最终证实CML可以通过释放外泌体对骨髓微环境进行"趋利避害"性改造，为深入理解CML进展机制及提高CML疗效提供理论基础。

The adhesion deficiency of BMSCs to hematopoietic cells is an important cause of the progression of CML and the failure of bone marrow transplantation, but the exactly mechanisms have not been fully elucidated. Our previous studies have found that the CML exosomes selectively carry high concentrations of miR-711. Further bioinformatical analyses indicate that the target genes of miR-711 are include adhesion molecules, such as CD44, CXCL12, CCR9 and CDH5. Based on these, we put forward the hypothesis that CML cell derived-exosomes may selectively transport miR-711 to down-regulate the expression of adhesion molecules in BMSCs and inhibit their adhesion function. We propose to apply series experiments, such as confocal microscopy, cell adhesion assay, non-contact in vitro co-culture assay and co-transplantation to mouse model, to confirm that exosomes have inhibitory effects on adhesion functions of BMSCs; and utilize luciferase assay, over-expression or knock-down of miR-711 in BMSCs, RT-PCR and Western blot to verify that exosomes achieve their inhibition function through miR-711 reducing the expression of adhesion molecules in BMSCs. This study will make a meaningful exploration for verifying the theory that CML cells may reconstruct the bone marrow microenvironment by shedding exosomes,and understanding of CML progress mechanism and improving the curative effect of CML.