AKAP12 positive fibroblast determines immunosuppressive contexture and immunotherapy response in patients with TNBC by promoting macrophage M2 polarization
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View abstract on PubMed
Summary
This summary is machine-generated.Cancer-associated fibroblasts expressing AKAP12 promote triple-negative breast cancer (TNBC) immune suppression and poor prognosis. Targeting IL-34 may improve immunotherapy for TNBC patients.
Area Of Science
- Oncology
- Immunology
- Cancer Biology
Background
- Triple-negative breast cancer (TNBC) is aggressive with poor prognosis.
- Cancer-associated fibroblasts (CAFs) significantly influence TNBC progression and treatment.
- Identifying specific CAFs subpopulations is crucial for understanding TNBC development.
Purpose Of The Study
- To identify CAFs subpopulations contributing to TNBC development.
- To investigate the role of AKAP12+ CAFs in the TNBC microenvironment.
- To explore AKAP12+ CAFs' association with immunotherapy response and prognosis.
Main Methods
- Multiomics analyses (cytometry by time-of-flight, RNA sequencing) were used.
- AKAP12+ CAFs and their clinical significance in 80 TNBC patients were assessed.
- Immunofluorescence assays elucidated the immune landscape and functional mechanisms.
Main Results
- An AKAP12+ CAFs subset associated with immunotherapy response was identified.
- High AKAP12+ CAFs population correlated with poor TNBC prognosis.
- AKAP12+ CAFs promote an immunosuppressive microenvironment via IL-34/CSF1R signaling, mediating macrophage M2 polarization.
Conclusions
- AKAP12+ CAFs are negatively associated with TNBC patient prognosis.
- AKAP12+ CAFs contribute to an immunosuppressive TNBC microenvironment by promoting M2 macrophage polarization.
- Targeting IL-34 shows potential to enhance TNBC immunotherapy efficacy.
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