乳腺癌细胞的转移与复发是乳腺癌病人死亡的主要原因，乳腺癌细胞的增殖失控则是其转移的生理基础。细胞自噬是维持细胞稳态的重要方式，自噬的活化与否与肿瘤的发生发展密切相关。抑癌因子EBP50可以通过调控PTEN信号通路等多种途径抑制乳腺癌的增殖与转移。我们发现EBP50能够有效调节乳腺癌细胞的自噬反应，这可能是其能够抑制乳腺癌细胞增殖与转移的重要途径，然而其详细地机制与作用仍需要进一步的阐明。本研究拟从探讨EBP50调节乳腺癌细胞MDA-MB-231以及MCF-7细胞株的自噬活性入手，使用构建稳定细胞系、免疫共沉淀等多种方法在细胞模型及动物模型对其进行研究，以期能够阐明EBP50通过PTEN通路及非依赖于PTEN通路两种方式激活自噬活性最终抑制乳腺癌增殖与转移的机制。我们的研究不仅有助深入了解乳腺癌的发生机制，而且可能发现针对乳腺癌的药物靶点，为开发新一代肿瘤防治药物提供理论基础。

In recent years, breast cancer is the most common malignancy and the leading cause of cancer mortality in women worldwide. The metastasis and recurrence of breast cancer is the main cause of death in breast cancer patients. And the excessive proliferation of cells is the physiological basis of breast cancer transfer. Autophagy, the important way to maintain cell homeostasis, is related with tumor development. EBP50, a multipotent scaffold protein, suppresses the proliferation and metastasis of breast cancer through a variety of ways, such as regulation of PTEN signaling pathway. We found that EBP50 could up-regulate the autophagic activity in breast cancer cells MDA-MB-231 and MCF-7, which may be an important manner to restrain metastasis and proliferation of breast cancer cell. However, the detailed relationship between EBP50-stimulating autophagy and proliferation and metastasis of breast cancer is unclear hithreto. In this project, we would like to futher explore the mechanism of how EBP50 stimulates the autophagy through PTEN pathway dependently or independently to suppress the development of proliferation and metastasis in breast cancer. The results driven from these studies will help us to identify therapeutic targets against tumorous diseases, such as breast cancer.