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Neutrophils and Neutrophil-Based Drug Delivery Systems in Anti-Cancer Therapy

Wahnou, Hicham, El Kebbaj, Riad, Hba, Soufyane, Ouadghiri, Zaynab, El Faqer, Othman, Pinon, Aline, Liagre, Bertrand, Limami, Youness, Duval, Raphaël Emmanuel·2025·Cancers
DOI 10.3390/cancers17071232PMC PMC11988188
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Abstract

Neutrophils, the most abundant white blood cells, play a dual role in cancer progression. While they can promote tumor growth, metastasis, and immune suppression, they also exhibit anti-tumorigenic properties by attacking cancer cells and enhancing immune responses. This review explores the complex interplay between neutrophils and the tumor microenvironment (TME), highlighting their ability to switch between pro- and anti-tumor phenotypes based on external stimuli. Pro-tumorigenic neutrophils facilitate tumor growth through mechanisms such as neutrophil extracellular traps (NETs), secretion of pro-inflammatory cytokines, and immune evasion strategies. They contribute to angiogenesis, tumor invasion, and metastasis by releasing vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs). Conversely, anti-tumor neutrophils enhance cytotoxicity by generating reactive oxygen species (ROS), promoting antibody-dependent cell-mediated cytotoxicity (ADCC), and activating other immune cells such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. Recent advances in neutrophil-based drug delivery systems have harnessed their tumor-homing capabilities to improve targeted therapy. Neutrophil-mimicking nanoparticles and membrane-coated drug carriers offer enhanced drug accumulation in tumors, reduced systemic toxicity, and improved therapeutic outcomes. Additionally, strategies to modulate neutrophil activity, such as inhibiting their immunosuppressive functions or reprogramming them towards an anti-tumor phenotype, are emerging as promising approaches in cancer immunotherapy. Understanding neutrophil plasticity and their interactions with the TME provides new avenues for therapeutic interventions. Targeting neutrophil-mediated mechanisms could enhance existing cancer treatments and lead to the development of novel immunotherapies, ultimately improving patient survival and clinical outcomes.

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Figure 1 Pro-tumorigenic functions of neutrophils: (A). recruitment to the TME, (B). Neutrophil Extracellular Traps (NETs), (C). secretion of pro-tumorigenic factors, (D). immunosuppressive activities, (E). facilitation of metastatic dissemination.
Figure 1 Pro-tumorigenic functions of neutrophils: (A). recruitment to the TME, (B). Neutrophil Extracellular Traps (NETs), (C). secretion of pro-tumorigenic factors, (D). immunosuppressive activities, (E). facilitation of metastatic dissemination.CC BY · PubMed Central
Figure 2 Anti-tumorigenic functions of neutrophils: (A). direct cytotoxicity, (B). Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC), (C); activation of other immune cells, and (D). anti-angiogenic activity.
Figure 2 Anti-tumorigenic functions of neutrophils: (A). direct cytotoxicity, (B). Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC), (C); activation of other immune cells, and (D). anti-angiogenic activity.CC BY · PubMed Central
Figure 3 Therapeutic strategies and mechanisms of action, targeting PMN-MDSCs: (A). inhibition of the immunosuppressive function of PMN-MDSCs, (B). blockade of PMN-MDSCs differentiation, (C). blockade of PMN-MDSCs recruitment and (D). PMN-MDSCs reduction.
Figure 3 Therapeutic strategies and mechanisms of action, targeting PMN-MDSCs: (A). inhibition of the immunosuppressive function of PMN-MDSCs, (B). blockade of PMN-MDSCs differentiation, (C). blockade of PMN-MDSCs recruitment and (D). PMN-MDSCs reduction.CC BY · PubMed Central
Figure 4 Synthesis of neutrophil membrane-mimetic drug delivery systems and their mechanisms of action: (A). artificial “super neutrophils” (GCZM), (B). platelet–neutrophil hybrid membrane-coated gold nanocages (PNMAuDIs), (C). pseudoneutrophil cytokine sponges (pCSs), (D). neutrophil-mimicking nanodevice (FKPN), (E). Nm@MSNs-DOX/SM nanocomplex, (F). neutrophil membrane-coated nanoparticles (TNM-PN), (G). neutrophil membrane-coated immunomagnetic nanoparticles (Neu-IMNs).
Figure 4 Synthesis of neutrophil membrane-mimetic drug delivery systems and their mechanisms of action: (A). artificial “super neutrophils” (GCZM), (B). platelet–neutrophil hybrid membrane-coated gold nanocages (PNMAuDIs), (C). pseudoneutrophil cytokine sponges (pCSs), (D). neutrophil-mimicking nanodevice (FKPN), (E). Nm@MSNs-DOX/SM nanocomplex, (F). neutrophil membrane-coated nanoparticles (TNM-PN), (G). neutrophil membrane-coated immunomagnetic nanoparticles (Neu-IMNs).CC BY · PubMed Central
Figure 5 Synthesis of neutrophil membrane-mimetic drug delivery systems and their mechanisms of action: (A). urease micromotor-powered neutrophils (UM-NEs) nanodrug delivery system, (B). paclitaxel-loaded liposomal neutrophils (PTX-CL/NEs), (C). CTX-NPs@NEs (cabazitaxel-loaded nanoparticles with neutrophils), (D). abraxane/human neutrophils cytopharmaceuticals, (E). neotype neutrophil cytopharmaceutical (NEs@STING-Mal-NP) with liposomal STING agonists, (F). neutrophil-based delivery system for Au nanorods (AuNR), (G). photoactive neutrophils (PAN) encapsulated multifunctional nanocomplex (RA/Ce6) of RGD apoptotic peptide conjugate (RA) decorated liposomal photosensitizer Ce6, (H). inflammation-activatable engineered neutrophils: Neutrophil/Dox-loaded MMSNs (ND-MMSNs), (I). nanoparticle–neutrophil composites (NSNP@Ne).
Figure 5 Synthesis of neutrophil membrane-mimetic drug delivery systems and their mechanisms of action: (A). urease micromotor-powered neutrophils (UM-NEs) nanodrug delivery system, (B). paclitaxel-loaded liposomal neutrophils (PTX-CL/NEs), (C). CTX-NPs@NEs (cabazitaxel-loaded nanoparticles with neutrophils), (D). abraxane/human neutrophils cytopharmaceuticals, (E). neotype neutrophil cytopharmaceutical (NEs@STING-Mal-NP) with liposomal STING agonists, (F). neutrophil-based delivery system for Au nanorods (AuNR), (G). photoactive neutrophils (PAN) encapsulated multifunctional nanocomplex (RA/Ce6) of RGD apoptotic peptide conjugate (RA) decorated liposomal photosensitizer Ce6, (H). inflammation-activatable engineered neutrophils: Neutrophil/Dox-loaded MMSNs (ND-MMSNs), (I). nanoparticle–neutrophil composites (NSNP@Ne).CC BY · PubMed Central

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Metadata

Authors
Wahnou, H., El Kebbaj, R., Hba, S., Ouadghiri, Z., El Faqer, O., Pinon, A., Liagre, B., Limami, Y., & Duval, R. E.
Venue
Cancers
Publisher
MDPI AG
Published
2025-04-05
Volume
17
Issue
7
Pages
1232
ISSN
2072-6694
DOI
10.3390/cancers17071232
PMC
PMC11988188
Cited by
35
References
8
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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