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

ABSTRACT: Stromal FOXF2 suppresses prostate cancer progression and metastasis by enhancing antitumor immunity

PROVIDER: PRJNA795664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17499154_1.fastq.gz	Fastqsanger.gz
	SRR17499154_2.fastq.gz	Fastqsanger.gz
	SRR17499155_1.fastq.gz	Fastqsanger.gz
	SRR17499155_2.fastq.gz	Fastqsanger.gz
	SRR17499156_1.fastq.gz	Fastqsanger.gz

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

Project description:We performed single cell RNA-Seq of FACS-isolated CD45+ leukocytes and Lin-CD24- prostate stromal cells from Col1a2-TRAMP(Control) group and Col1a2-Foxf2-TRAMP group. Unsupervised clustering analysis on integrated single-cell datasets revealed an increased CD8+ T cell frequency and activity and a decreased Macrophage and MDSC activity in the Col1a2-Foxf2-TRAMP mice. The analysis in TRAMP mice revealed two major subpopulations that represented the myofibroblastic CAF (myCAF) and inflammatory CAF (iCAF). The percentage of myCAF increased by 15% in the Col1a2-Foxf2-TRAMP mice, suggesting that Foxf2 induced a shift toward the myCAF phenotype. On the other hand, the overall CAF gene signature score defined by the average expression of 30 CAF-associated genes on a single cell level was slightly but significantly reduced in the Col1a2-Foxf2-TRAMP mice.

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

Project description: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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Project description:To identify the genes and pathways regulated by FOXF2, we investigated potential FOXF2 gene targets by microarray analyses of primary prostate stromal cells (PrSC) in which FOXF2 was knocked down by siRNA. 190 differentially expressed genes were selected, of which 104 genes were more highly expressed in PrSC cells treated with FOXF2 siRNA and 86 were more highly expressed in PRSC cells treated with negative control siRNA. Experiment Overall Design: In each experiment, we compared gene expression of PrSC cells treated with FOXF2 siRNA versus PrSC cells treated with negative control siRNA, in a total of 6 affymetrix arrays. 190 differentially expressed genes were selected (ratio negative control siRNA/siRNA â¥ 2log |0.8| as average in all arrays).

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