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Identifying FOXA1-GR transcriptional targets in FOXA1-GR dependent NSCLC

ABSTRACT: Identifying FOXA1-GR transcriptional targets in FOXA1-GR dependent NSCLC

PROVIDER: PRJNA838217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19214001_1.fastq.gz	Fastqsanger.gz
	SRR19214001_2.fastq.gz	Fastqsanger.gz
	SRR19214002_1.fastq.gz	Fastqsanger.gz
	SRR19214002_2.fastq.gz	Fastqsanger.gz
	SRR19214003_1.fastq.gz	Fastqsanger.gz

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Identifying FOXA1-GR transcriptional targets in FOXA1-GR dependent NSCLC

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

Characterization of ER, GR, and FoxA1 binding patterns in breast cancer cells treated with either Dex or E2

Project description:The estrogen receptor (ER), glucocorticoid receptor (GR), and forkhead box protein 1 (FoxA1) are significant factors in breast cancer progression. FoxA1 is well-established as a pioneer factor for steroid receptor recruitment to chromatin. Here we show that ER and GR have the ability to alter the genomic response of FoxA1 to specific binding sites within the genome. These findings alter the classical understood mechanism of FoxA1 establishing a dynamic transcription factor that can be regulated by hormones.

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Novel assays monitoring direct GR protein activity exhibit high predictive power for ligand activity on endogenous GR gene targets

Project description:Exogenous glucocorticoids are widely used in the clinic for the treatment of inflammatory disorders and auto-immune diseases. Unfortunately, their use is hampered by many side effects and therapy resistance. Efforts to find more selective glucocorticoid receptor (GR) agonists and modulators (called SEGRAMs), able to separate anti-inflammatory effects via gene suppression from metabolic effects via gene activation, have been unsuccessful so far. In this study, we characterized a set of functionally diverse GR ligands in A549 cells, first using a panel of luciferase-based reporter gene assays evaluating GR-driven gene activation and gene suppression. We expanded this minimal assay set with novel luciferase-based read-outs monitoring GR protein levels, GR dimerization and GR Serine 211 (Ser211) phosphorylation status and compared their outcomes with compound effects on the mRNA levels of known GR target genes in A549 cells and primary hepatocytes. We found that luciferase reporters evaluating GR-driven gene activation and gene repression were not always reliable predictors for effects on endogenous target genes. Remarkably, our novel assay monitoring GR Ser211 phosphorylation levels proved to be the most reliable predictor for compound effects on almost all tested endogenous GR targets, both driven by gene activation and repression. The integration of this novel assay in existing screening platforms may therefore increase chances to find novel GR ligands with an improved therapeutic benefit.

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Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer (ChIP-Seq)

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