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Background <p>Neutrophils are the most abundant circulating leukocytes and are raipidly recruited to inflammatory sites as key effectors of innate immunity. Nasopharyngeal carcinoma (NPC), an Epstein–Barr virus (EBV)-associated epithelial malignancy endemic in Southeast Asia and North Africa, develops within a chronically inflamed and immunologically specialized tumor microenvironment (TME). Current standard therapies (concurrent chemoradiotherapy and induction chemotherapy) face challenges of recurrence and metastasis, highlighting the need to explore the role of neutrophils in NPC progression and potential therapeutic targets.</p> Main body <p>EBV shapes the cytokine/chemokine milieu in the NPC TME, driving neutrophil recruitment and reprogramming into a continuum of tumor-associated neutrophils (TANs) and PMN-MDSC–like states. These neutrophils promote tumor progression via immunosuppression, extracellular matrix remodeling, angiogenesis, and metastasis. Neutrophil extracellular traps (NETs) further mediate immune evasion, thrombosis, and dissemination. Clinically, peripheral inflammatory indices correlate with NPC prognosis but are limited by heterogeneous cutoffs and confounding factors. Neutrophils also exhibit context-dependent anti-tumor effects. Potential therapies include targeting the CXCL8–CXCR1/2 axis, modulating NET formation, and combining with immune checkpoint inhibitors.</p> Conclusions <p>This review establishes a unifying framework linking EBV-driven inflammation to neutrophil plasticity, NET biology, and NPC progression. Neutrophils are dynamic, targetable components with dual pro-tumor and anti-tumor roles. While neutrophil-related indices hold prognostic value, their clinical translation requires standardization and integration with other biomarkers. Targeting suppressive neutrophil programs and NETs offers promising strategies to improve therapeutic efficacy and overcome treatment resistance in NPC.</p>

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Neutrophils in nasopharyngeal carcinoma: from mechanisms to therapeutics

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月7日

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  • Wenlin Liu,
  • Bo You,
  • Zongshuai Miao,
  • Jiaxuan Yu,
  • Xinran Ding,
  • Chenyan Zhou

摘要

Background

Neutrophils are the most abundant circulating leukocytes and are raipidly recruited to inflammatory sites as key effectors of innate immunity. Nasopharyngeal carcinoma (NPC), an Epstein–Barr virus (EBV)-associated epithelial malignancy endemic in Southeast Asia and North Africa, develops within a chronically inflamed and immunologically specialized tumor microenvironment (TME). Current standard therapies (concurrent chemoradiotherapy and induction chemotherapy) face challenges of recurrence and metastasis, highlighting the need to explore the role of neutrophils in NPC progression and potential therapeutic targets.

Main body

EBV shapes the cytokine/chemokine milieu in the NPC TME, driving neutrophil recruitment and reprogramming into a continuum of tumor-associated neutrophils (TANs) and PMN-MDSC–like states. These neutrophils promote tumor progression via immunosuppression, extracellular matrix remodeling, angiogenesis, and metastasis. Neutrophil extracellular traps (NETs) further mediate immune evasion, thrombosis, and dissemination. Clinically, peripheral inflammatory indices correlate with NPC prognosis but are limited by heterogeneous cutoffs and confounding factors. Neutrophils also exhibit context-dependent anti-tumor effects. Potential therapies include targeting the CXCL8–CXCR1/2 axis, modulating NET formation, and combining with immune checkpoint inhibitors.

Conclusions

This review establishes a unifying framework linking EBV-driven inflammation to neutrophil plasticity, NET biology, and NPC progression. Neutrophils are dynamic, targetable components with dual pro-tumor and anti-tumor roles. While neutrophil-related indices hold prognostic value, their clinical translation requires standardization and integration with other biomarkers. Targeting suppressive neutrophil programs and NETs offers promising strategies to improve therapeutic efficacy and overcome treatment resistance in NPC.