复发与转移是乳腺癌患者死亡的主要原因，而上皮-间质转化（EMT）是导致乳腺癌细胞获得高转移能力的重要机制。大量证据显示自噬在EMT的发生发展中扮演了重要的角色并已成为肿瘤治疗的潜在靶标，然而其具体机制尚未完全揭示。BOK作为近年来新发现的抑癌基因，在肿瘤发展中的作用尚不明确。我们前期发现BOK在促进乳腺癌细胞自噬的同时抑制了EMT的发生，提示BOK在自噬及EMT调控中具有关键作用，其机制仍需深入研究。本项目拟在前期工作基础上，通过临床、动物及细胞水平阐明BOK通过促进自噬抑制EMT及转移的分子机制。本研究不仅为阐明乳腺癌自噬与EMT的关系提供一定的理论基础，同时有助于揭示乳腺癌中BOK低表达促进侵袭转移的作用机制，为进一步开发乳腺癌的药物靶点提供新策略。

Recurrence and metastasis are the main causes of death in patients with breast cancer, and epithelial-mesenchymal transformation (EMT) is an important mechanism that lead to high metastatic ability of breast cancer cells. A large number of evidence shows that autophagy plays an important role in the occurrence and development of EMT and has become a potential target for tumor treatment. However, its specific mechanism has not yet been fully revealed. As a newly discovered tumor suppressor gene in recent years, the role of BOK in tumor development is not clear. We found that BOK not only promoted autophagy but also inhibited the occurrence of EMT in breast cancer cells, suggesting that BOK plays a key role in autophagy and EMT regulation, and its mechanism still needs to be further studied. Based on previous work, this project intends to elucidate the molecular mechanism of BOK which inhibite EMT and metastasis by promoting autophagy at the clinical, animal and cellular levels. This study not only provides a theoretical basis for elucidating the relationship between autophagy and EMT in breast cancer, but also helps to reveal the mechanism of low expression of BOK in breast cancer to promote invasion and metastasis, and also provides a new strategy for the further development of drug targets in breast cancer.