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Chronic inflammation is known to be associated with prostate cancer development, but how epithelium-associated cancer-initiating events cross talk to inflammatory cells during prostate cancer initiation and progression is largely unknown. Using thePten null murine prostate cancer model, we show an expansion of Gr-1+ CD11b+ myeloid-derived suppressor cells (MDSCs) occurring intraprostatically immediately following epithelium-specificPten deletion without expansion in hematopoietic tissues. This MDSC expansion is accompanied by sustained immune suppression. Prostatic Gr-1+ CD11b+ cells, but not those isolated from the spleen of the same tumor-bearing mice, suppress T cell proliferation and express high levels ofArginase 1 andiNOS . Mechanistically, the loss of PTEN in the epithelium leads to a significant upregulation of genes within the inflammatory response and cytokine-cytokine receptor interaction pathways, includingCsf1 andIl1b , two genes known to induce MDSC expansion and immunosuppressive activities. Treatment ofPten null mice with the selective CSF-1 receptor inhibitor GW2580 decreases MDSC infiltration and relieves the associated immunosuppressive phenotype. Our study indicates that epithelium-associated tumor-initiating events trigger the secretion of inflammatory cytokines and promote localized MDSC expansion and immune suppression, thereby promoting tumor progression.

molecular and cellular biology

<i>Pten</i> Null Prostate Epithelium Promotes Localized Myeloid-Derived Suppressor Cell Expansion and Immune Suppression during Tumor Initiation and Progression

Pten Null Prostate Epithelium Promotes Localized Myeloid-Derived Suppressor Cell Expansion and Immune Suppression during Tumor Initiation and Progression