自噬与肿瘤的关系是目前研究的热点。最近项目组发现小分子化合物RITA激活p53通过多种信号通路诱导B系恶性肿瘤细胞凋亡，同时伴有自噬中心信号通路哺乳动物雷帕霉素受体（mTOR）底物分子4EBP1下降；且文献报道RITA增加了白血病细胞化疗药物的敏感性。本项目在上述研究基础上，提出Rita参与诱导白血病细胞自噬发生的假说，这一过程参与调节白血病细胞化疗敏感性。针对上述假说，本项目拟采用RNA干扰、免疫共沉淀、Western blot、流式细胞技术、电镜分析、激光共聚焦图像分析等研究手段，从多方面进一步深入系统的探讨Rita对主要的自噬信号通路（PI3K-I/AKT/mTOR，Beclin1复合物）的影响，进而揭示其通过自噬调节白血病细胞化疗药物敏感性的分子机制。开展本项目可望揭示Rita在白血病自噬中的作用，为白血病治疗提供新的思路和实验线索。

At present a research hotspot is to explore the relationship of autophagy and tumor. We report that RITA by reactivation of p53 induced the apoptosis of B hematological malignancies cells， and the downregulation of mTOR substrates, 4EBP1 at the same time.And reported in the literature that RITA enhances the chemosensivity of leukemia cells.Therefore,we put forward the hypothesis that RITA induces autophagy of leukemia cells,and it regulates chemosensivity of leukemia cells.Concerning the hypothesis,we will adopt several research method including RNA interfere, Co-Immunoprecipitation analysis, Western blot, flow cytometric analysis, Transmission electron microscopy analysis, Laser confocal image analysis, and so on,to probe the effects of RITA on autophagic signal pathway(PI3K-I/AKT/mTOR, Beclin1 complex).Further,we will reveal the mechanism of leukemia cells' chemosensivity of autophagic regulation.To carry out the project,the effect of RITA on leukemia autophagy will be revealed in order to supply new train of thought and experimental clues.