Effect of FOXA1 over-expression upon AR binding in AR-driven cancers
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR307344.fastq.gz | Fastqsanger.gz | |||
| ERR307345.fastq.gz | Fastqsanger.gz | |||
| ERR307346.fastq.gz | Fastqsanger.gz | |||
| ERR307347.fastq.gz | Fastqsanger.gz | |||
| ERR307348.fastq.gz | Fastqsanger.gz |
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Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.
2014-01-14 | E-MTAB-1749 | biostudies-arrayexpress
Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. ChIP_Seq examination of AR, FoxA1 and GATA2 binding sites in LNCaP and DU145 cells
2016-01-11 | E-GEOD-69043 | biostudies-arrayexpress
Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. genetic_modification_design
2016-01-11 | E-GEOD-69044 | biostudies-arrayexpress
Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability.
2016-01-11 | GSE69044 | GEO
Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability.
2016-01-11 | GSE69043 | GEO
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
2024-05-01 | GSE232124 | GEO
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
2024-05-01 | GSE232123 | GEO
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
2024-05-01 | GSE232122 | GEO
Project description:Approximately 75% of breast cancers are driven by the estrogen receptor alpha (ER), and despite the advent of endocrine therapy to block ER signaling pathways, a significant portion of women develop resistance to these drugs. The pioneer factor FOXA1 has been shown to facilitate nearly all DNA-binding events of ER in response to estrogen in ER+ breast cancer (ER+BC). Notably, up-regulation of FOXA1 is a hallmark of endocrine-resistant phenotypes and has been shown to reprogram enhancer elements, leading to an altered transcriptome. However, FOXA1 is a critical pioneer factor for multiple nuclear hormone receptors aside from ER and is implicated in regulation of important factors such as HER2 and the androgen receptor (AR). With the diverse array of breast cancer molecular subtypes displaying complex interplay between ER, HER2, AR, PR, and other hormone receptors, describing the complete ensemble of FOXA1 binding partners in various contexts, such as endocrine-resistant tumors, is of increasing importance. To classify FOXA1 interactors, we generated MCF-7 cell lines stably expressing the biotin ligase miniTurbo fused to the N- or C-terminus of FOXA1. Using proximity labeling (PL) coupled with LC-MS/MS, we have comprehensively cataloged interactors of FOXA1, including expected proteins such as ER, AR, MLL3, YAP1, and GATA-3. Moreover, we have discovered 157 previously unpublished interactors of FOXA1. Importantly, poorer prognosis for relapse-free survival among ER+BC patients is associated with several of these novel interactors, including NR2C2, an orphan nuclear receptor previously shown to regulate various nuclear hormone receptor signaling but whose roles in breast cancer remain unclear. NR2C2 ChIP-seq in MCF-7 cells under control or FOXA1-depleted conditions revealed multiple NR2C2 binding mechanisms in relation to FOXA1 levels and binding, suggesting possible coordinate regulation of key loci. Integrating proteomic and genomic approaches, we have potentially highlighted new mechanisms of FOXA1 that could have future clinical impacts.
2025-10-06 | PXD046652 | Pride
Project description:The FOXA1 pioneer factor is an essential mediator of steroid receptor function in multiple hormone dependent cancers, including breast and prostate cancers, enabling nuclear receptors such as ER and AR to activate lineage specific growth programs. . Analyzing data from loss-of-function screens, we identified a subset of NSCLC tumor lines where proliferation is FOXA1-dependent. Using rapid immunoprecipitation and mass spectrometry of endogenous protein (RIME) we identified chromatin-localized interaction between FOXA1 and glucocorticoid receptor (GR) in these tumor cells. Knockdown of GR inhibited proliferation of FOXA1-dependent, but not FOXA1-independent NSCLC cells. Here, we utilized ChIP-sequencing to identify a permissive set of genes potentially regulated by FOXA1 and GR to understand potential mechanisms underlying FOXA1-GR dependence in NSCLC.
2022-05-16 | GSE203036 | GEO