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Stromal FOXF2 suppresses prostate cancer progression and metastasis by enhancing antitumor immunity. | LitMetric

AI Article Synopsis

  • Cancer-associated fibroblasts (CAFs) have an immunosuppressive effect on tumors, but the mechanisms are not fully understood; this study highlights the role of the Foxf2 protein in the stroma of prostate cancer.
  • Increasing levels of Foxf2 in prostatic stroma suppress tumor growth and progression by reducing the immunosuppressive CAF phenotype and improving T cell activity.
  • The presence of Foxf2 correlates with better outcomes in prostate cancer, as its higher expression is linked to lower Gleason grades and may explain the rarity and slower progression of cancers in the transition zone of the prostate.

Article Abstract

Cancer-associated fibroblasts (CAFs) mediate an immunosuppressive effect, but the underlying mechanism remains incompletely defined. Here we show that increasing prostatic stromal Foxf2 suppresses the growth and progression of both syngeneic and autochthonous mouse prostate cancer models in an immunocompetent context. Mechanistically, Foxf2 moderately attenuates the CAF phenotype and transcriptionally downregulates Cxcl5, which diminish the immunosuppressive myeloid cells and enhance T cell cytotoxicity. Increasing prostatic stromal Foxf2 sensitizes prostate cancer to the immune checkpoint blockade therapies. Augmenting lung stromal Foxf2 also mediates an immunosuppressive milieu and inhibits lung colonization of prostate cancer. FOXF2 is expressed higher in the stroma of human transition zone (TZ) than peripheral zone (PZ) prostate. The stromal FOXF2 expression level in primary prostate cancers inversely correlates with the Gleason grade. Our study establishes Foxf2 as a stromal transcription factor modulating the tumor immune microenvironment and potentially explains why cancers are relatively rare and indolent in the TZ prostate.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9652358PMC
http://dx.doi.org/10.1038/s41467-022-34665-zDOI Listing

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