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FOXA1 suppresses cancer immunity independent of DNA binding

ABSTRACT: FOXA1 suppresses cancer immunity independent of DNA binding

PROVIDER: PRJNA596242 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR10721400_1.fastq.gz	Fastqsanger.gz
	SRR10721400_2.fastq.gz	Fastqsanger.gz
	SRR10721401_1.fastq.gz	Fastqsanger.gz
	SRR10721401_2.fastq.gz	Fastqsanger.gz

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FOXA1 suppresses cancer immunity independent of DNA binding

Project description:Exclusion of lymphocytes from tumors is a major barrier for effective immuno- and chemo-therapy of cancer. We found that FOXA1 overexpression inversely correlates with expression of antigen processing and presentation and interferon signaling genes in different cancer types. FOXA1 binds to STAT proteins and inhibits expression of antigen presentation and interferon response genes and tumor immunity independent of the forkhead domain - DNA binding function. Increased FOXA1 also correlates with immunotherapy resistance in murine triple negative breast tumor and bladder cancer in patients and chemo-resistance in breast cancer patients. Our results reveal that FOXA1 is a key immune suppressor, suggesting that FOXA1 overexpression may predict tumor resistance to immuno- and chemo-therapies and that depletion of FOXA1 may therapeutically convert cancers from ‘immune-cold’ to ‘immune-hot’ diseases.

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Binding of the pioneer factor FOXA1 is independent of hormonal signalling

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Binding of the pioneer factor FOXA1 is independent of hormonal signalling

Project description:We hormone deprived MCF-7 and ZR75-1 breast cancer cells for three days and treated them with vehicle (ethanol) or estrogen for 45 minutes. We then performed FOXA1 ChIP-seq and showed that the vast majority (>99%) of FOXA1 binding events are not affected by steroid conditions. A small number (<1%) of FOXA1 binding sites appear to be induced by estrogen, but these are not genuine de novo binding sites and represent ‘shadow’ binding sites that result from chromatin interactions at super-enhancer containing estrogen-regulated genomic regions. FOXA1 is therefore not regulated by estrogen and remains a bone fide therapeutic target that is entirely upstream of the ER complex.

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Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells

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Androgen receptor-independent function of FoxA1 in prostate cancer metastasis

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated engineered LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression. We performed microarray analysis of these cells. We performed microarray analysis on LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression

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SETDB1-TRIM28 complex suppresses antitumor immunity

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Androgen receptor-independent function of FoxA1 in prostate cancer metastasis

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated engineered LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression. We performed microarray analysis of these cells.

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