肿瘤无限生长特性是其细胞凋亡受抑制的结果，研究肿瘤细胞凋亡的分子调控机制，通过诱导肿瘤细胞凋亡来治疗肿瘤，是临床治疗的目标之一。课题组前期实验发现PGC-1β与FOXA2存在相互作用关系，推测其通过LKB1/AMPK/mTOR信号通路调控乳腺癌干细胞的增殖。为了验证该推测，采用人乳腺癌细胞系和裸鼠乳腺荷瘤模型为对象，分别进行：①GST pull-down、Co-IP、激光共聚焦、缺失突变体检测，验证PGC-1β与FOXA2的作用关系及其亚细胞定位；② Western blot、流式细胞术、裸鼠成瘤等，探讨PGC-1β与FOXA2共表达对乳腺癌细胞凋亡的影响；③与LKB1/AMPK/mTOR信号通路相关的基因和蛋白分析，明确PGC-1β与FOXA2在促进乳腺肿瘤细胞凋亡的分子机制。研究结果将为阐明PGC-1β协同FOXA2调控乳腺肿瘤干细胞凋亡的分子机制，及对乳腺癌靶向临床治疗研究提供基础。

The immortal characteristics of tumor cells are the result of cell apoptosis inhibition, and this apoptosis inhibition is regulated by multiple genes and cell signaling pathways. Many scientists have been trying to investigate the mechanisms of the signaling pathway that regulates cell apoptosis, hoping to find molecules that could be used to antagonize apoptosis resistance, with the hope to induce tumor cell apoptosis as a better way for tumor therapy.In the previous experiment, our research group found the interaction between PGC-1β and FOXA2 for the first time, which through the mTOR/AKT signaling pathway in breast cancer stem cell proliferation. To test this hypothesis, we used the human breast cancer cells and breast cancer in nude mice animal model through the following experimental validation. 1) We used the GST pull-down, Co-IP, confocal laser, PGC-1βdeletion mutant and subcellular localization to detect the interaction. 2) We used Western blot, flow cytometry, nude mice tumor formation to investigate the PGC-1β and FOXA2 co-expression on the growth of breast cancer cell. 3) Through the LKB1/AMPK/mTOR signal pathway analysis, we detected the proliferation of breast cancer cells between PGC-1βand FOXA2, which lay the basement for targeted clinical treatment of breast cancer.