ArticleBMC medicine2026
Targeting ADGRG1 in cancer-associated adipocytes reprograms the immunosuppressive microenvironment and enhances immunotherapy responsiveness in triple-negative breast cancer models.
Article in BMC medicine, 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
backgroundThe adipocyte-rich microenvironment of the breast plays a crucial role in tumor progression, yet the functional heterogeneity of cancer-associated adipocytes (CAAs) and their specific mechanisms in driving immunosuppressive microenvironment and therapy resistance remain inadequately characterized.
methodsWe performed an integrated analysis of single-nucleus RNA sequencing (snRNA-seq) data from human adipose tissue and bulk transcriptomic data from the TCGA-BRCA and METABRIC cohorts. A prognostic signature was developed based on transcriptional features of CAA subpopulations. Functional roles of the key gene ADGRG1 were investigated through in vitro co-culture systems and in vivo breast cancer models using genetic knockdown/overexpression and pharmacological inhibition.
resultssnRNA-seq revealed a distinct CAA subpopulation enriched in aggressive contexts, labeled as HAD7. The HAD7-based signature stratified patients into high- and low-score groups, with the high-score group exhibiting poor survival and an immunosuppressive microenvironment. ADGRG1 was identified as a core driver. In vitro, ADGRG1 in CAAs promoted cancer cell migration, invasion, and epithelial mesenchymal transition. In vivo, adipocyte-specific ADGRG1 enhanced tumor growth, metastasis, and impaired anti-tumor immunity. Mechanistically, ADGRG1 activated a CXCL8-AKT/mTOR signaling axis. Crucially, pharmacological inhibition of ADGRG1 synergized with anti-PD-1 therapy, effectively suppressing tumor growth and metastasis by reversing immunosuppressive microenvironment.
conclusionsOur study identifies ADGRG1 as a master regulator of a pro-tumorigenic CAA subpopulation. Targeting the ADGRG1-CXCL8-AKT/mTOR axis represents a promising stromal-targeting strategy to overcome immunotherapy resistance in breast cancer.
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