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Regulatory cistrome landscape of Foxa1 and Foxa2 during prostate cancer progression [ChIP-seq]

ABSTRACT: Regulatory cistrome landscape of Foxa1 and Foxa2 during prostate cancer progression [ChIP-seq]

PROVIDER: PRJNA789935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17267003_1.fastq.gz	Fastqsanger.gz
	SRR17267003_2.fastq.gz	Fastqsanger.gz
	SRR17267004_1.fastq.gz	Fastqsanger.gz
	SRR17267004_2.fastq.gz	Fastqsanger.gz
	SRR17267005_1.fastq.gz	Fastqsanger.gz

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Regulatory cistrome landscape of Foxa1 and Foxa2 during prostate cancer progression [ChIP-seq]

Project description:To characterize the genome-wide regulatory cistrome of Foxa1 and Foxa2, we performed both Foxa1 and Foxa2 chromatin immunoprecipitation followed by sequencing (ChIP-seq) on freshly dissociated prostate tumor cells at the early stage (2 weeks post tamoxifen administration) and the late stage (6 months post tamoxifen administration) of NEPC progression, respectively.

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Project description:FOXA1 and FOXA2 are essentail transcription factors for proper gut development. In adults, they have a role in the differentiation of intestinal secretory cell lineages and were also reporeted to directly activate Muc2 transcription. Here we show that deletion of Foxa1 and Foxa2 in mouse intestinal epithelium leads to a downregulation of glycosylation genes in the colon and to a massive change of the colonic surface glycans. In turn, the microbiome composition shifts dramatically and spontaneous inflammatory bowel disease ensued. We conclude that vertebrates shape a favorable microbiome by establishing a glycocalyx to nurture specific bacterial taxa through control of the epithelial glycosylation program by the FoxA transcription factors.

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Project description:Uterine glands are central to endometrial function and fertility, however the mechanisms regulating their development and function are not well understood. The pioneer forkhead box A2 (FOXA2) transcription factor is distinctively expressed in the glands of the endometrium in both the human and mouse uterus. Studies in mice established that FOXA2 is a critical regulator of gland development in the neonatal uterus as well as differentiated gland function in the adult uterus. An integrative approach was used here to define the FOXA2 cistrome in the human endometrium. Genome-wide mapping of FOXA2 binding sites by chromatin immunoprecipitation sequencing (ChIP-Seq) was performed on proliferative (P) and mid-secretory (MS) phase endometrium and combined with the transcriptome determined by RNA sequencing (RNA-Seq). Distinctive binding of FOXA2 was observed between the P and MS endometrium, and FOXA2 binding intervals were enriched for different transcription factor binding motifs between the phases of endometrium. Pathway analysis revealed different biological processes regulated by FOXA2 bound genes in the P and MS endometrium. Thus, FOXA2 is proposed to regulate gene expression in concert with other transcription factors to influence gland function in a cycle phase-dependent manner. Further analysis identified potential FOXA2 regulated genes that influence endometrial growth, uterine receptivity, and stromal cell decidualization. This analysis of the FOXA2 cistrome provides a foundation essential to understanding fundamental aspects of uterine gland development, differentiation, function, and disease.

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Foxa1 and Foxa2 are Required for Sexual Dimorphism in Liver Cancer - Gene Expression

Project description:Gene expression changes between livers of treated WT and dKO (Foxa1 and Foxa2 KO) male and female mice and untreated female (WT and dKO) mice were measured to identify pathways related to Foxa1/2 regulation of pathways involved in liver cancer. The experiment uses 4 replicates each for 6 conditions

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Gene expression profiles of Foxa1 and Foxa2 single and double mutants in embryonic mouse liver

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Foxa1 and Foxa2 are Required for Sexual Dimorphism in Liver Cancer - Gene Expression

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FOXA1 and FOXA2 binding profile in mouse colon [ChIP]

Project description:FOXA1 and FOXA2 are essentail transcription factors for proper gut development. In adults, they play a role in the differentiation of intestinal secretory cells and were also reporeted to directly activate Muc2 transcription. Here we show that FOXA1 and FOXA2 bind near goblet cell genes, and are specifically enriched near glycosylation genes. Deletion of these transcription factors in mouse intestine leads to a downregulation of glycosylation genes in the colon and to a massive change of the colonic surface glycans. I turn, the microbiome composition shifts dramatically and spontaneous inflammatory bowel disease ensued. We conclude that vertebrates shape a favorable microbiome by establishing a glycocalyx to nurture specific bacterial taxa through control of the epithelial glycosylation program by the FoxA transcription factors.

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Project description:Changes in cellular identity (also known as histologic transformation or lineage plasticity) can drive malignant progression and resistance to therapy in multiple types of cancer, including lung adenocarcinoma (LUAD). The lineage specifying transcription factors FoxA1 and FoxA2 (FoxA1/2) regulate identity in NKX2-1/TTF1-negative LUAD. However, their role in NKX2-1-positive LUAD has not been systematically investigated. We find that Foxa1/2 knockout severely impairs tumorigenesis in KRAS-driven genetically engineered mouse models and human cell lines. Foxa1/2 deletion leads to collapse of a dual-identity state, marked by co-expression of pulmonary and gastrointestinal transcriptional programs, that has been implicated in LUAD progression. Mechanistically, loss of FoxA1/2 leads to aberrant NKX2-1 activity and genomic localization, which inhibits tumorigenesis and drives alternative cellular identity programs associated with non-proliferative states. This work demonstrates that FoxA1/2 expression is a novel lineage-specific vulnerability in NKX2-1-positive LUAD and identifies mechanisms of response and resistance to targeting FoxA1/2 in this disease.

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Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer

Project description:Foxa1loxP/loxP;Foxa2loxP/loxP and Foxa1loxP/loxP;Foxa2loxP/loxP;AfpCre mice of both genders were treated with or without carcinogen to induce liver cancer. ChIP-Seq was performed in the liver samples after cross-linking. ChIP-DNA was sequenced with the Illumina GAII sequencer. The AfpCre when present knocks out the Foxa1 and Foxa2 genes, so removing the corresponding proteins.

2012-02-24 | E-MTAB-805 | biostudies-arrayexpress

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