骨髓血管新生增加是多发性骨髓瘤发病及进展的关键，MSCs是骨髓微环境中的一种重要细胞成分，我们前期研究发现MSCs参与了多发性骨髓瘤的耐药,但在血管新生中作用尚不明确。本课题拟通过研究MSCs在多发性骨髓瘤血管新生中作用，为骨髓瘤血管新生机制的基础研究开辟新领域。ILK与肿瘤转移、耐药、血管形成和细胞分化密切相关，ILK参与了肿瘤细胞和内皮细胞介导的血管新生，在上皮细胞和成纤维细胞分化中发挥重要调控作用。我们前期研究发现ILK在多发性骨髓瘤耐药中具有重要作用，但ILK是否参与了多发性骨髓瘤MSCs介导的血管新生，其机制如何尚无相关研究报道。本课题拟通过RNA干扰技术下调ILK表达或重组腺病毒过表达ILK，观察其对多发性骨髓瘤MSCs分泌血管生成因子及分化为血管内皮细胞、平滑肌细胞及相关信号途径影响，阐明ILK在MSCs介导的多发性骨髓瘤血管新生中作用，为多发性骨髓瘤抗血管生成治疗寻找新靶点

Angiogenesis plays a crucial role in the pathogenesis and progression of multiple myeloma.Mesenchymal stem cells(MSCs) are important elements of bone marrow enviroments. Our previous studies showed that MSCs are involved in the drug resistance of multiple myeloma. To date, the role of MSCs in the angiogenesis of multiple myeloma has not been elucidated. In this study, the role of MSCs in the angiogenesis of multiple myeloma was investigated to elucidate a new mechanism of angiogenesis of myeloma. Integrin-linked kinase(ILK) is closely correlated with metastasis, drug resistance and angiogenesis of various cancers and diferentiation of cells.Previous studies indicated that ILK was involved in the angiogenesis mediated by solid tumor cells and endothelial cells. Our previous studies showed that MSCs played vital roles in the drug resistance of multiple myeloma.In addition, ILK is a key mediator in the control of myofibroblast and mammary epithelial differentiation.The role of ILK in the angiogenesis of multiple myeloma and the related mechanism has not been investigated by now. In this research,small interfering RNA and recombinant adenovirus overexpressing ILK were used respectively,to investigate the effect of ILK on the secretion of angiogenic factors and differentiation into endothelial cells and smooth muscle cells by MSCs and the related signal pathway. This study will establish a rationale for anti-angiogenesis therapy by targeting ILK and provided a new strategy for multiple myeloma..