ArticleCancer immunology, immunotherapy : CII2026
CXCL1-overexpressing cancer-associated fibroblasts stimulate hepatocellular carcinoma progression via neutrophil recruitment, NET formation, and immune suppression.
Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Immunosuppressive tumor microenvironment and immunotherapy resistance of esophageal carcinoma.Frontiers in immunology · 2026Review
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6 authors.
Funding
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Abstract
backgroundHepatocellular carcinoma (HCC) is a highly aggressive malignancy with a prognosis often limited by an immunosuppressive tumor microenvironment (TME). While cancer-associated fibroblasts (CAFs) are known to influence tumor progression, the specific mechanisms by which they modulate immune cell recruitment and function remain poorly defined. This study investigates how CAF-derived CXCL1 orchestrates a pro-tumorigenic stroma through neutrophil manipulation.
methodsThe study employed in vitro co-culture systems and in vivo murine models to evaluate the impact of CXCL1-overexpressing CAFs on HCC progression. The signaling mechanisms were assessed using CXCR2 and STAT3 inhibitors, while immune surveillance was monitored via CD8+ T cell activity and natural killer (NK) cell infiltration assays.
resultCXCL1 secreted by CAFs was found to activate neutrophils via the CXCR2-STAT3 signaling axis. This activation induces the formation of neutrophil extracellular traps (NETs), which directly facilitate tumor proliferation and metastasis. Furthermore, CXCL1-driven NETs established a potent immunosuppressive TME by significantly impairing CD8+ T cell activity and reducing NK cell infiltration. Conversely, neutralizing CXCL1 or inhibiting the CXCR2-STAT3 pathway successfully suppressed NET formation, restored anti-tumor immune cell functionality, and mitigated tumor growth.
conclusionsThe 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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