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Lucicebtide (ST101) effect on hPBMCs-derived M2-type macrophages.

GSE288861 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/02/10 Platform GPL34284
Summary
Reprogramming immunosuppressive M2-like macrophage to immune-active M1-like macrophage represents a promising strategy to improve responses to immunotherapy. Lucicebtide (previously referred to as ST101) is a peptide antagonist of the transcription factor C/EBPβ, a key activator of the transcriptional program in immunosuppressive macrophages. We show that Lucicebtide exposure reprograms human Perypheral Blood Mononuclear cells (hPBMSc)-derived M2-like macrophage to the pro-inflammatory M1-like phenotype. RNAseq tracriptional profiling of M2-like macrophages untreated or treated with Lucicebtide induces a substantial dowregulation of the M2-program and a subset of known C/EBPβ targets. Taken togheter, these data highlight the ability of Lucicebtide to rewire the M2-like immunosuppressive program and support combinatorial stategies to potentiate immunotherapy approaches.
Published in
The C/EBPβ antagonist peptide lucicebtide (ST101) induces macrophage polarization toward a pro-inflammatory phenotype and enhances anti-tumor immune responses
Scuoppo C, Ramirez R, Leong SF et al. · Frontiers in immunology 2025 · PMID 40103809 · doi:10.3389/fimmu.2025.1522699
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Also filed as BioProject PRJNA1219646 and SRA study SRP561828. Searching any of these in the dataset finder brings you back here.

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