Title: Abstract B029: Foxf2 activates antitumor immunity to repress the progression of prostate cancer by repressing Fgl1
Abstract: Abstract Targeting immune suppressive mechanisms in the tumor microenvironment has revolutionized cancer treatment. Although immune checkpoint inhibition (ICI) has yielded meaningful responses across many cancer types, the ICI efficacy is still limited for prostate cancer. We generated a mouse model with prostate epithelial specific expression of Foxf2, a Forkhead box transcription factor. Foxf2 overexpression suppressed tumor growth in two mouse models for prostate cancer with prostate specific Pten deletion or TRAMP. Foxf2 expression strongly induced tumor cell-intrinsic immune responses by recruiting and activating CD8+ T cells and switching the polarization of macrophages from an immunosuppressive M2-like phenotype to a more inflammatory M1-like state in both syngeneic and autochthonous mouse prostate cancer models in an immunocompetent context. Furthermore, we showed that overexpression of Foxf2 in mouse and human prostate cells repressed the expression of FGL1, a major ligand of LAG-3 that mediates T cell suppression. In this study, we take a combination of bioinformatic, molecular, cellular, and genetic approaches and reveal that Foxf2 overexpression in prostate cancer suppresses tumor progression by activating antitumor immunity. Citation Format: Deyong Jia, Zhicheng Zhou, OhJoon Kwon, Li Xin. Foxf2 activates antitumor immunity to repress the progression of prostate cancer by repressing Fgl1 [abstract]. In: Proceedings of the AACR Special Conference: Advances in Prostate Cancer Research; 2023 Mar 15-18; Denver, Colorado. Philadelphia (PA): AACR; Cancer Res 2023;83(11 Suppl):Abstract nr B029.
Publication Year: 2023
Publication Date: 2023-06-02
Language: en
Type: article
Indexed In: ['crossref']
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