ArticleTranslational cancer research2026
MIF-mediated intercellular crosstalk drives antigen-presenting-like cancer-associated fibroblast differentiation in triple-negative breast cancer via TGF-β signaling.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Triple-negative breast cancer (TNBC) is characterized by an aggressive tumor microenvironment (TME) in which cancer-associated fibroblasts (CAFs) play a pivotal role. However, the molecular mechanisms governing the transformation of quiescent fibroblasts into distinct CAF subtypes within TNBC remain poorly understood. This study aimed to elucidate the molecular mechanisms underlying fibroblast-to-CAF subtype transition in TNBC and identify key signaling pathways involved in TNBC-driven CAF activation. Methods: Transcriptomic data from The Cancer Genome Atlas (TCGA)-TNBC were analyzed using weighted gene co-expression network analysis (WGCNA). CAF-related scores and TNBC scores were computed via single-sample gene set enrichment analysis (ssGSEA). CAF infiltration was assessed using Estimating the Proportion of Immune and Cancer cells (EPIC). Survival and correlation analyses were validated in the Gene Expression Omnibus (GEO) dataset GSE58812. Single-cell RNA sequencing (scRNA-seq) data (GSE176078) were employed for cell-type annotation, pseudotime trajectory inference, and cell-cell communication analysis. Cell experiments were further performed to explore the mechanisms of fibroblast activation in TNBC. Results: TNBC score was significantly associated with poor prognosis and positively correlated with CAF score/infiltration. Single-cell analysis revealed antigen-presenting CAFs (apCAFs) as the predominant CAF subtype in TNBC. Pseudotime trajectory analysis showed that 96 genes uniquely involved in quiescent-to-apCAF-like differentiation were enriched in TGF-β signaling. Cell-cell communication analysis identified macrophage migration inhibitory factor (MIF)-(CD74 + CXCR4) as significantly enhanced during TNBC-apCAF interactions but absent in TNBC-myofibroblastic CAF (myCAF) crosstalk. Four hub genes, including Conclusions: A TNBC-to-apCAF signaling axis was identified wherein TNBC-secreted MIF activates CD74/CXCR4 on fibroblasts, engaging TGF-β signaling to drive apCAF-like differentiation. These findings offer potential therapeutic targets for disrupting the pro-tumorigenic microenvironment in TNBC.
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