预转移巢（PMN）是肿瘤转移的先决条件。破坏PMN可以显著抑制肿瘤转移。骨髓来源的细胞通常被招募到预转移器官以支持PMN的形成，这可以通过肿瘤分泌的因子来组织。中性粒细胞能够趋化性地迁移至炎症部位并消耗肿瘤分泌的因子，可以作为广谱抑制PMN形成和转移的治疗药物。然而，中性粒细胞在对炎症信号做出反应时可能释放中性粒细胞外围陷阱（NETs），促进肿瘤转移。在本研究中，通过快速冷冻处理将活性中性粒细胞转化为死亡中性粒细胞（C NE），以保持其靶向PMN和消耗肿瘤分泌因子的能力，但消除NET释放的缺点。考虑到巨噬细胞在PMN中对细胞外基质的重塑作用，细菌磁体矿（Mag）进一步搭载在C NE的表面上形成C NEMag，可以将巨噬细胞从M2极性转化为M1极性，进一步破坏PMN形成。一系列的体外和体内评估已经应用来确认C NEMag在抑制PMN形成和转移方面的有效性。本研究提出了一种有前景的靶向抗转移治疗策略。本文受版权保护。版权所有。

Pre-metastatic niche (PMN) is a prerequisite for tumor metastasis. Destruction of PMN can significantly suppress the tumor metastasis. Bone marrow-derived cells are usually recruited into the pre-metastatic organs to support PMN formation, which can be orchestrated by tumor-derived secreted factors. Neutrophils can chemotactically migrate towards the inflammatory sites and consume tumor-derived secreted factors, capable of acting as therapeutic agents for a broad-spectrum suppression of PMN formation and metastasis. However, neutrophils in response to inflammatory signals can release neutrophil extracellular traps (NETs), promoting the tumor metastasis. Herein, live neutrophils were converted into dead neutrophils (C NE) through a quick-frozen process to maintain PMN-targeting and tumor-derived secreted factor-consuming abilities but eliminate NET-releasing shortcoming. Considering macrophages-regulated remodeling of the extracellular matrix in PMN, bacterial magnetosomes (Mag) were further hitchhiked on the surface of C NE to form C NEMag , which could repolarize macrophages from M2 to M1 phenotype for further disruption of PMN formation. A series of in vitro and in vivo assessments have been applied to confirm the effectiveness of C NEMag in suppression of PMN formation and metastasis. This study presents a promising strategy for targeted anti-metastatic therapy in clinics. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.