Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 - PubMed
3 hours ago
- #tumor metastasis
- #high endothelial venules
- #immune evasion
- Tumor-associated high endothelial venules (HEVs) act as a specific portal for tumor metastasis in lymph nodes, distinct from other blood vessels.
- Tumor involvement in HEVs serves as an independent prognostic marker in patients with lymph node-positive female breast cancer.
- Tumor cells spreading via HEVs exhibit reduced immunogenicity and greater capability for distant metastasis compared to those using non-HEV blood vessels.
- Mechanistically, tumor-derived SEMA3C promotes ALOX12 expression in HEVs, leading to production of the metabolite 12-HETE.
- 12-HETE binds selectively to ADAR1 p150, inducing phase separation and increasing A-to-I RNA editing in tumor cells, thereby reducing immune recognition of dsRNA and enabling immune evasion.