多发性骨髓瘤（multiple myeloma，MM）系浆细胞恶性克隆性疾病，目前发病率逐年增高且仍不可治愈。RAB7A是调控胞内囊泡与溶酶体融合的重要蛋白，参与受体内吞和自噬等基本生命活动过程。本课题组前期研究结果显示，敲除MM细胞株U266 RAB7A基因能阻断CXCR4的内吞和影响自噬导致LC3-II增加。本研究拟前期工作基础上，通过MM细胞株、免疫缺陷小鼠荷瘤模型进一步研究RAB7A在MM细胞增殖与凋亡中的作用，及相关的关键信号模块改变，探索RAB7A对MM细胞基因组稳定性的影响及可能的机制，从转录调控和信号转导水平深入揭示RAB7A调控骨髓瘤细胞的机制。课题如期完成有助于加深对骨髓瘤发病机制的理解，也能为多发性骨髓瘤防治提供新的潜在靶点和策略。

Multiple myeloma (MM) is a currently incurable plasma malignancy and the incidence goes up annually. There is one of feasible methods to explore new targets and strategy for the treatment of MM from the regulation of differentiation and survival of plasma cells. RAB7A is an important protein that regulates the integration of intracellular vesicles with lysosomes and participates in basic life activities such as endocytosis and autophagy.Our previous research has shown that knockout of MM cell line U266 RAB7A gene could block CXCR4 endocytosis and affect autophagy lead to increased LC3-II. Based on the previous work, the further study will focus on the role of RAB7A in MM cell proliferation and apoptosis , the related key signal pathway and the possible mechanisms on the genomic stability of MM cells from the transcription and signal transduction level using myeloma cell lines, immunodeficient mouse tumor model .The project deadline helps to deepen the understanding of the pathogenesis of MM, and also can offer new potential targets and strategy for prevention and control of MM.