Cell membrane derived liposomes loaded with DNase I target neutrophil extracellular traps which inhibits colorectal cancer liver metastases

Wang, Zhaozhong; Chen, Chen; Shi, Chongdeng; Zhao, Xiaotian; Gao, Lin; Guo, Feiyue; Han, Maosen; Yang, Zhenmei; Zhang, Jing; Tang, Chunwei; Zhang, Cai; Liu, Ying; Sun, Peng; Jiang, Xinyi

doi:10.1016/j.jconrel.2023.04.013

Cited by 21 publications

(4 citation statements)

References 39 publications

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“…Furthermore, the deposition and light‐controlled cargo release from systemic delivery of AuPB@mPDA carriers in livers, abolishes NETs‐based capture of CTCs as well as metastatic spread. Cell membrane derived liposomes encapsulated with DNase I efficiently recruit neutrophils and eliminate NETs, eventually hindering CRC liver metastases 174 . Doxorubicin‐loaded micellar low‐molecular‐weight‐heparin‐astaxanthin nanoparticles decrease the recruitment of neutrophils in livers and MDSCs in lungs and breast tumors and suppress NF‐κB‐STAT3 signaling, thus preventing breast cancer hepatic metastasis via suppressing NETs formation as well as suppressing pulmonary metastasis and alleviating the inflammatory and immunosuppressive TME 175 .…”

Section: Emerging Nanoplatforms For Improving the Efficacy Of Antinet...mentioning

confidence: 99%

NETosis: Sculpting tumor metastasis and immunotherapy

Hu,

Wang,

Liu

2023

Immunological Reviews

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SummaryThe process of neutrophil extracellular traps (NETs) formation, called NETosis, is a peculiar death modality of neutrophils, which was first observed as an immune response against bacterial infection. However, recent work has revealed the unique biology of NETosis in facilitating tumor metastatic process. Neutrophil extracellular traps released by the tumor microenvironment (TME) shield tumor cells from cytotoxic immunity, leading to impaired tumor clearance. Besides, tumor cells tapped by NETs enable to travel through vessels and subsequently seed distant organs. Targeted ablation of NETosis has been proven to be beneficial in potentiating the efficacy of cancer immunotherapy in the metastatic settings. This review outlines the impact of NETosis at almost all stages of tumor metastasis. Furthermore, understanding the multifaceted interplay between NETosis and the TME components is crucial for supporting the rational development of highly effective combination immunotherapeutic strategies with anti‐NETosis for patients with metastatic disease.

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Section: Emerging Nanoplatforms For Improving the Efficacy Of Antinet...mentioning

confidence: 99%

NETosis: Sculpting tumor metastasis and immunotherapy

Hu,

Wang,

Liu

2023

Immunological Reviews

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“…While DNase I could cause impaired host defense against infection, tumor specific delivery and release of DNase I in tumor sites breaks NET-mediated physical barrier and increases the contact of cytotoxic T cells and sensitizes immune checkpoint blockade therapy in CRC ( 135 ). Biomimetic CCDC25-overexpressing cell membrane hybrid liposomes loaded with DNase I efficiently eliminates NETs and inhibits CRC liver metastasis ( 136 ). PAD4 inhibitors include Cl-amindine, GSK484, YW3-56 and some other peptide-based inhibitors.…”

Section: Clinical Applications Of Nets and Gut Microbiota In Crcmentioning

confidence: 99%

Crosstalk between gut microbiota and metastasis in colorectal cancer: implication of neutrophil extracellular traps

Wu,

Dong,

Pan

et al. 2023

Front. Immunol.

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Primary colorectal cancer (CRC) often leads to liver metastasis, possibly due to the formation of pre-metastatic niche (PMN) in liver. Thus, unravelling the key modulator in metastasis is important for the development of clinical therapies. Gut microbiota dysregulation is a key event during CRC progression and metastasis. Numerous studies have elucidated the correlation between specific gut bacteria strains (e.g., pks+E. coli and Bacteroides fragilis) and CRC initiation, and gut bacteria translocation is commonly witnessed during CRC progression. Gut microbiota shapes tumor microenvironment (TME) through direct contact with immune cells or through its functional metabolites. However, how gut microbiota facilitates CRC metastasis remains controversial. Meanwhile, recent studies identify the dissemination of bacteria from gut lumen to liver, suggesting the role of gut microbiota in shaping tumor PMN. A pro-tumoral PMN is characterized by the infiltration of immunosuppressive cells and increased pro-inflammatory immune responses. Notably, neutrophils form web-like structures known as neutrophil extracellular traps (NETs) both in primary TME and metastatic sites, NETs are involved in cancer progression and metastasis. In this review, we focus on the role of gut microbiota in CRC progression and metastasis, highlight the multiple functions of different immune cell types in TME, especially neutrophils and NETs, discuss the possible mechanisms of gut microbiota in shaping PMN formation, and provide therapeutical indications in clinic.

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“…Given the critical role of the surface protein CCDC25 in tumor cell binding to NETs, Jiang et al prepared biomimetic CCDC25 overexpressing cell membranefused liposomes to directly target NETs. 19 Torchilin et al designed micelles modified with the monoclonal antibody 2C5 to recognize the histones of NETs and achieved specific degradation of NETs. 20 Of note, biomimetic methods and monoclonal antibodies are expensive, limiting their widespread use.…”

Section: Introductionmentioning

confidence: 99%

A Two-Pronged Delivery Strategy Disrupting Positive Feedback Loop of Neutrophil Extracellular Traps for Metastasis Suppression

Kong,

Deng,

et al. 2024

ACS Nano

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Neutrophil extracellular traps (NETs) severely affect tumor metastasis through a self-perpetuating feedback loop involving two key steps: (1) mitochondrial aerobic respiration-induced hypoxia promotes NET formation and (2) NETs enhance mitochondrial metabolism to exacerbate hypoxia. Herein, we propose a two-pronged approach with the activity of NET-degrading and mitochondrion-damaging by simultaneously targeting drugs to NETs and tumor mitochondria of this loop. In addition to specifically recognizing and eliminating extant NETs, the NET-targeting nanoparticle also reduces NET-induced mitochondrial biogenesis, thus inhibiting the initial step of the feedback loop and mitigating extant NETs' impact on tumor metastasis. Simultaneously, the mitochondrion-targeting system intercepts mitochondrial metabolism and alleviates tumor hypoxia, inhibiting neutrophil infiltration and subsequent NET formation, which reduces the source of NETs and disrupts another step of the self-amplifying feedback loop. Together, the combination significantly reduces the formation of NET− tumor cell clusters by disrupting the interaction between NETs and tumor mitochondria, thereby impeding the metastatic cascade including tumor invasion, hematogenous spread, and distant colonization. This work represents an innovative attempt to disrupt the feedback loop in tumor metastasis, offering a promising therapeutic approach restraining NET-assisted metastasis.

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Cell membrane derived liposomes loaded with DNase I target neutrophil extracellular traps which inhibits colorectal cancer liver metastases

Cited by 21 publications

References 39 publications

NETosis: Sculpting tumor metastasis and immunotherapy

NETosis: Sculpting tumor metastasis and immunotherapy

Crosstalk between gut microbiota and metastasis in colorectal cancer: implication of neutrophil extracellular traps

A Two-Pronged Delivery Strategy Disrupting Positive Feedback Loop of Neutrophil Extracellular Traps for Metastasis Suppression

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