三阴性乳腺癌易复发转移缺乏有效治疗靶点，是当前的研究热点。文献报道，Rab27蛋白介导肿瘤细胞释放外泌体传输CSF-1使肿瘤微环境中巨噬细胞极化并释放表皮生长因子调控肿瘤细胞mTOR信号通路。课题组前期研究发现三阴性乳腺癌mTOR通路上游因子EGFR与EGF结合可调控下游因子磷酸化促进其发生发展。预实验显示，三阴性乳腺癌细胞Rab27蛋白表达明显上调，外泌体含量增多体积增大，两者呈正相关关系。因此，拟以三阴性乳癌Rab27蛋白为研究对象，通过体内外实验调控Rab27蛋白介导外泌体分泌影响肿瘤相关巨噬细胞释放EGF，以期减少肿瘤微环境中EGF与该信号通路上游分子EGFR的结合，抑制该通路下游分子Akt、p21的异常磷酸化水平，达到抑制三阴性乳腺癌细胞增殖活性的目的。探讨调控Rab27蛋白介导外泌体分泌对三阴性乳腺癌mTOR信号通路的影响机制，为寻找治疗靶点提供实验数据、奠定理论基础。

The lack of effective treatment target for the easy recurrence and metastasis of three- negative breast cancer is a hot research topic at present. It is reported that Rab27 protein mediates tumor cells to release external secretion CSF-1 so that macrophages in tumor microenvironment polarization and released EGF to regulate tumor cell mTOR signaling pathway. In the early study of our group, it was found that the combination of the upstream factor EGFR and EGF in the mTOR pathway of three-negative breast cancer could regulate the downstream factor phosphorylation and promote its development. The pre-experiment showed that the expression of Rab27 protein in three-negative breast cancer cells increased obviously, and the volume of exosomes increased , and the relationship beteewn the two were positively correlated. Therefore, it is proposed to use three-negative breast cancer Rab27 protein as the research object, by regulating Rab27 protein mediated the secretion of exosomes influence tumor associated macrophages release EGF, in order to ruduce the combination of EGF in tumor-microenvironment and the upstream molecular EGFR of mTOR pathway, inhibit the downstream molecular Akt of the pathway and the abnormal phosphorylation level of p21 was aimed at inhibiting the proliferative activity of three-negative breast cancer cells. To explore the mechanism of regulating the effect of Rab27 protein mediated the secretion of exosome on mTOR signaling pathway in three-negative breast cancer, and to provide experimental data and theoretical basis for finding therapeutic targets.