ArticleInternational dental journal2026
CCR7 Promotes Neutrophil Recruitment and N2 Polarization Through Regulation of IL-16 in Head and Neck Squamous Cell Carcinoma.
Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- MMP1 Modulates Head and Neck Squamous Cell Carcinoma Progression and Therapeutic Response Via Tumour Microenvironment.International dental journal · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesWhile CCR7 is a known driver of head and neck squamous cell carcinoma (HNSCC) progression and tumour-associated neutrophils (TANs) are key microenvironmental mediators, the role of CCR7 in regulating TAN recruitment and pro-tumorigenic N2 polarization remains unknown. This study aimed to delineate this novel regulatory axis.
methodsBioinformatic analyses of TCGA and HPA datasets were performed to evaluate clinical associations among CCR7 expression, neutrophil infiltration, and N2 polarization markers in HNSCC. Mechanistic insights were obtained from in vitro models using conditioned medium from HNSCC cell lines (FADU, PCI-37B) to study CCR7/IL-16-mediated recruitment and polarization of neutrophil-like HL-60 cells. The functional effects of these N2-polarized neutrophils on HNSCC proliferation and invasion were also quantified.
resultsHigh CCR7 expression in HNSCC correlated with elevated neutrophil infiltration and N2 polarization markers. CCR7 knockdown suppressed neutrophil recruitment (P < .01) and N2 polarization (P < .001). Mechanistically, CCR7 signalling regulated IL-16 secretion, which mediated neutrophil chemotaxis and N2 polarization (P < .05). These N2-polarized neutrophils promoted a pro-tumorigenic feedback loop, enhancing HNSCC proliferation, migration, and invasion (P < .01).
conclusionThese findings establish CCR7 as a key regulator of IL-16-mediated neutrophil recruitment and N2 polarization in HNSCC, highlighting its potential as a therapeutic target to remodel the immunosuppressive tumour microenvironment.
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