CEBPB-high dormant tumor cells drive immune evasion via S100A8 orchestrated tumor-associated macrophages reprogramming - PubMed
4 days ago
- #CEBPB
- #Immune Evasion
- #Tumor Dormancy
- CEBPB-high dormant tumor cells drive immune evasion in Triple Negative Breast Cancer (TNBC).
- Dormant tumor cells resist immune checkpoint blockade (ICB) therapy and reside in an immunosuppressive niche.
- CEBPB maintains tumor dormancy by activating cell cycle negative regulators like CCNG2.
- CEBPB orchestrates a tumor-supportive microenvironment by recruiting and polarizing M2 macrophages and suppressing T cells.
- S100A8 is a key transcriptional target of CEBPB that promotes M2 macrophage polarization.
- Targeting CEBPB or S100A8 can overcome ICB resistance and remodel the tumor microenvironment.
- The CEBPB-S100A8 axis is a promising therapeutic target to enhance ICB efficacy in TNBC.