Histone lactylation increases CXCL1 expression for neutrophil infiltration and immune escape in pancreatic cancer - PubMed
3 months ago
- #immunotherapy
- #histone lactylation
- #pancreatic cancer
- Histone lactylation (H3K18la) increases CXCL1 expression, promoting neutrophil infiltration and immune escape in pancreatic cancer.
- Glycolysis-derived lactate induces H3K18la, upregulating CXCL1, which recruits neutrophils and induces immunosuppression.
- PCAF functions as a histone lactyltransferase, activating CXCL1 expression.
- Combination therapy with bromosporine (PCAF inhibitor) and anti-PD-1 antibody shows synergistic antitumor effects in pancreatic cancer models.
- The study identifies the Lactate-PCAF-H3K18la-CXCL1 pathway as a mechanism for neutrophil infiltration and immunosuppression in pancreatic cancer.