Findings demonstrate that CAFs promote HCC progression by recruiting neutrophils and aiding immune suppression, suggesting new therapeutic targets.
The CXCL1-CXCR2-STAT3 axis is a critical driver of stromal-immune interactions in HCC. By mediating neutrophil recruitment and NET-driven immune evasion, CAFs create a permissive environment for tumor escalation. Targeting this signaling pathway represents a promising therapeutic strategy to disrupt pro-tumorigenic neutrophil mechanisms and reinvigorate the host's anti-tumor immunity.
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Bi et al. (2026) studied this question.
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