ArticleCancer discovery2026
Dual Functions of B7-H3-MAPK Signaling Orchestrate Tumor Immunosuppression via Regulating the Plasticity of Myeloid-derived Suppressor Cells and Fibroblasts.
Article in Cancer discovery, 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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Authors and funding
16 authors.
Funding
Abstract
B7-H3/CD276 is an emerging immunotherapy target in cancers. However, limited knowledge of B7-H3 signaling and its role in modulating the tumor microenvironment hinders the clinical application of B7-H3-targeting therapy. Here, we report that B7-H3 plays dual roles in regulating myeloid-derived suppressor cells (MDSCs) and cancer-associated fibroblasts (CAFs), thereby promoting tumor progression and therapy resistance, respectively. We comprehensively characterized a non-canonical function of B7-H3 that triggers MAPK signaling in monocytic MDSCs and induces cellular senescence. The senescent monocytic M-MDSCs secreted chemokines to recruit immunosuppressive granulocytic MDSCs. Genetic deletion or pharmacological inhibition of B7-H3/Cd276 reduced Gr-MDSCs and delayed tumor progression. Nevertheless, the secretory factor SPINK1 derived from MDSCs compensatorily activates EGFR/MEK/ERK signaling in CAFs and promotes their extracellular matrix remodeling features, dampening B7-H3-targeting immunotherapy. Combining the B7-H3 monoclonal antibody with the FDA-approved MEK inhibitor trametinib showed durable anti-tumor effects in preclinical models of castration-resistant prostate cancer by fully attenuating immunosuppressive mechanisms.
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Registered trials
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