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Migration and homing of dendritic cells (DCs) to lymphoid organs are quite crucial for T cell-induced immune response against tumor. However, tumor microenvironment can make some tumor cells escape immune response by impairing DC migration. Prostaglandin E 2  (PGE 2 ) plays important roles in initiating and terminating inflammatory responses. In this study, we investigated whether PGE 2  could inhibit murine prostate cancer progression by countervailing tumor microenvironment-induced impairment of dendritic cell migration. We found that murine prostate cancer cell line RM-1-conditioned medium impaired chemotactic movement of marrow-derived DCs and splenic cDCs toward CC chemokine receptor-7 (CCR7) ligand CCL19 in vitro and migration to draining lymph gland in vivo. Meanwhile, it also induced LXR α  activation and CCR7 inhibition on maturing DCs. However, the treatment of PGE 2  rescued this impairment of DC migration with upregulation of CCR7 and inhibition of LXR α . Further, it was observed that PGE 2  also increased MMP9 expression and activated Notch1 signaling on DCs. In RM-1-bearing mouse model, PGE 2  treatment was identified to inhibit tumor growth and induce more tumor-infiltrating T cells and CD11c dendritic cells in tumor sites. Therefore, our findings may demonstrate a new perspective for therapeutic interventions on prostate cancer immunoescape.

journal of immunology research

Prostaglandin E<sub>2</sub> Inhibits Prostate Cancer Progression by Countervailing Tumor Microenvironment-Induced Impairment of Dendritic Cell Migration through LXR<i>α</i>/CCR7 Pathway

Prostaglandin E2 Inhibits Prostate Cancer Progression by Countervailing Tumor Microenvironment-Induced Impairment of Dendritic Cell Migration through LXRα/CCR7 Pathway

Prostaglandin E₂ Inhibits Prostate Cancer Progression by Countervailing Tumor Microenvironment-Induced Impairment of Dendritic Cell Migration through LXRα/CCR7 Pathway