如何延缓三阴性乳腺癌（TNBC）早期进展是亟需解决的临床问题，中性粒细胞外陷阱网（NETs）可能在TNBC进展中扮演重要角色。我们已发表研究结果证实FOXM1和miR-26b均与TNBC进展密切相关，预实验又首次发现NETs可使蛋白Merlin磷酸化后抑制Hippo通路，共同参与TNBC进展，但具体机制不详。我们提出如下假说：TNBC内中性粒细胞活化并释放NETs，通过膜受体TLR-9使Merlin磷酸化后抑制Hippo通路，其下游效应蛋白YAP与转录因子FOXM1结合后进入核内，共同抑制miR-26b成熟，使miR-26b下游一系列癌基因编码蛋白表达上调，最终形成反馈环路，参与TNBC进展。我们将从细胞实验、动物实验和临床标本三个层次展开研究，阐明NETs通过Hippo通路调控Merlin/FOXM1/miR-26b信号轴参与TNBC进展的具体机制，为TNBC临床治疗提供新思路和新靶点。

It is significant to reduce the early progression of triple negative breast cancer (TNBC) in clinical practice. Neutrophil extracellular traps (NETs) may play a significant role in the progression of TNBC. We have reported that FOXM1 and miR-26b are associated with TNBC progression. Our preliminary experiment results show that NETs in TNBC can phosphorylate Merlin and then inhibit Hippo signaling pathway. NETs are involved in the progression of TNBC, but the specific mechanism remains unknown. Therefore, we hypothesize that activated neutrophils in TNBC tissue release NETs, which phosphorylates Merlin and inhibits Hippo signaling pathway via the membrane receptor TLR-9. The effector protein YAP binds to the transcription factor FOXM1 and then they enter into nucleus, in which they inhibit the mature of miR-26b together and up-regulate the expression of proteins encoded by a series of oncogenes in the downstream of miR-26b. We will conduct the study from three levels, including in vitro and in vivo experiments and clinical specimen tests, to clarify the mechanism of NETs involvement in the progression of TNBC by regulating Merlin/FOXM1/ mir-26b axis via Hippo pathway, and finally to provide new ideas and new targets for the treatment of TNBC.