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FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer.

ABSTRACT: FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer.

PROVIDER: PRJNA957681 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24226043_1.fastq.gz	Fastqsanger.gz
	SRR24226043_2.fastq.gz	Fastqsanger.gz
	SRR24226044_1.fastq.gz	Fastqsanger.gz
	SRR24226044_2.fastq.gz	Fastqsanger.gz
	SRR24226045_1.fastq.gz	Fastqsanger.gz

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FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [RNA-seq]

Project description:Breast cancer biology varies markedly among patients. Basal-like breast cancer is one of the most challenging subtypes to treat because it lacks effective therapeutic targets. Despite numerous studies on potential targetable molecules in this subtype, few targets have shown promise. However, the present study revealed that FOXD1, a transcription factor that functions in both normal development and malignancy, is associated with poor prognosis in basal-like breast cancer. We analyzed publicly available RNA sequencing data and conducted FOXD1-knockdown experiments, finding that FOXD1 maintains gene expression programs that contribute to tumor progression. We first conducted survival analysis of patients grouped via a Gaussian mixture model based on gene expression in basal-like tumors, finding that FOXD1 is a prognostic factor specific to this subtype. Furthermore, our RNA sequencing and chromatin immunoprecipitation sequencing experiments on the basal-like breast cancer cell lines BT549 and Hs578T with FOXD1 knockdown revealed that FOXD1 regulates enhancer-gene programs related to tumor progression. These findings suggest that FOXD1 plays an important role in basal-like breast cancer progression and may represent a promising therapeutic target.

2023-04-25 | GSE230118 | GEO

FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [ChIP-seq]

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FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [ChIP-seq]

Project description:FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [ChIP-seq]

| PRJNA957692 | ENA

FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [RNA-seq]

Project description:FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer [RNA-seq]

| PRJNA957693 | ENA

FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer.

Project description:Breast cancer biology varies markedly among patients. Basal-like breast cancer is one of the most challenging subtypes to treat because it lacks effective therapeutic targets. Despite numerous studies on potential targetable molecules in this subtype, few targets have shown promise. However, the present study revealed that FOXD1, a transcription factor that functions in both normal development and malignancy, is associated with poor prognosis in basal-like breast cancer. We analyzed publicly available RNA sequencing data and conducted FOXD1-knockdown experiments, finding that FOXD1 maintains gene expression programs that contribute to tumor progression. We first conducted survival analysis of patients grouped via a Gaussian mixture model based on gene expression in basal-like tumors, finding that FOXD1 is a prognostic factor specific to this subtype. Then, our RNA sequencing and chromatin immunoprecipitation sequencing experiments using the basal-like breast cancer cell lines BT549 and Hs578T with FOXD1 knockdown revealed that FOXD1 regulates enhancer-gene programs related to tumor progression. These findings suggest that FOXD1 plays an important role in basal-like breast cancer progression and may represent a promising therapeutic target.

| S-EPMC10206236 | biostudies-literature

FOXD1 is associated with poor outcome and maintains tumor-promoting enhancer-gene programs in basal-like breast cancer.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-04-25 | GSE230119 | GEO

Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer

Project description:Elevated Met receptor tyrosine kinase (RTK) expression correlates with poor outcome in breast cancer, yet a causal role for Met in the development of breast cancer has not been directly established. To examine this question, we generated a transgenic mouse model that targets expression of an oncogenic Met receptor (MetMut) to the mammary epithelium. We show that MetMut induces mammary tumors with a variety of histopathologies that exhibit gene expression profiles sharing similarities with human basal and luminal breast tumor subtypes. Among all breast cancers, we further demonstrate that the Met receptor is primarily overexpressed in human basal and HER2 positive breast cancers, and that a Met associated gene expression signature identifies patients with poor prognosis. Keywords: Met, mammary, poor outcome, EMT, basal breast cancer

2009-03-30 | GSE10450 | GEO

Effect of Foxd1 knockdown in the reprogramming process

Project description:It remains unclear how the ectopic expression of defined transcription factors induces dynamic changes in gene expression profiles that establish a pluripotent state during direct cell reprogramming. In the present study, we first identified a temporal gene expression program during the reprogramming process. Promoter analyses then predicted the role of two forkhead box transcription factors, Foxd1 and Foxo1, as mediators of the gene expression program. Knockdown of Foxd1 or Foxo1 reduced the number of induced pluripotent stem cells (iPSCs). The knockout of Foxd1 prevented the downstream transcription program, including the expression of reprogramming marker genes. Interestingly, the expression level of Foxd1 was also transiently increased in a small population of cells in the middle stage of reprogramming. The presence or absence of Foxd1 expression in this stage was correlated with a future cell fate as iPSCs or non-reprogrammed cells. These results suggest that Foxd1 is a mediator and indicator of the successful progression of the gene expression program in cell reprogramming. Mouse embryonic fibroblasts (MEFs) of Foxd1+/+, Foxd1+/- or Foxd1-/- were infected with retroviruses encoding the three transcription factors (Oct4, Sox2 and Klf4) at day 0 and sampled at day 8.

2014-01-11 | E-GEOD-51179 | biostudies-arrayexpress

FOXD1 Promotes Dedifferentiation and Vemurafenib-resistance in Melanoma by Regulating the Expression of CTGF

Project description:Metastatic melanoma is the most aggressive skin cancer and associated with a poor prognosis. Targeted therapy is one of the most important treatments for patients with BRAFV600E-mutated advanced melanoma. However, the development of resistance to this treatment compromises its therapeutic success. Increasing evidence has indicated that NC-associated genes play important roles in tumor progress and drug resistance. Our previous study showed that FOXD1 is a neural crest (NC)-associated gene that has high expression levels both in NC cells and melanoma and that it could regulate melanoma migration and invasion. Here, we found that the FOXD1-CTGF axis is important for melanoma resistance. The connective tissue growth factor (CTGF) was identified as a direct downstream factor of FOXD1 using microarray assay. In detail, when we compared the microarray data from FOXD1 OE and control groups, we found that the expression level of CTGF was also higher in FOXD1 OE cells (FC=1.97).

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Effect of Foxd1 knockdown in the reprogramming process

2014-01-11 | GSE51179 | GEO