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FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [RNA-Seq]

ABSTRACT: FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [RNA-Seq]

PROVIDER: PRJNA1040817 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26841229_1.fastq.gz	Fastqsanger.gz
	SRR26841229_2.fastq.gz	Fastqsanger.gz
	SRR26841230_1.fastq.gz	Fastqsanger.gz
	SRR26841230_2.fastq.gz	Fastqsanger.gz
	SRR26841231_1.fastq.gz	Fastqsanger.gz

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FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma

Project description:FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma

| PRJNA1040818 | ENA

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [HiChIP]

Project description:FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [HiChIP]

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FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [Bisulfite-Seq]

Project description:FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [Bisulfite-Seq]

| PRJNA1040822 | ENA

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [ChIP-seq]

Project description:FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [ChIP-seq]

| PRJNA1040816 | ENA

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [HiChIP]

Project description:The ability of cancer cells to alter their identity is essential for tumor survival and progression. Loss of the pulmonary lineage specifier NKX2-1 within KRAS-driven lung adenocarcinoma (LUAD) enhances tumor progression and results in a pulmonary-to-gastric lineage switch that is dependent upon the activity of pioneer factors FoxA1 and FoxA2; however, the underlying mechanism remains largely unknown. Here, we show that FoxA1/2 reprogram the epigenetic landscape of NKX2-1-negative LUAD to facilitate a gastric differentiation program. Using sequential recombination models, we find that FoxA1/2 are required for demethylation of gastric-defining genes after Nkx2-1 deletion. FoxA1 colocalizes with TET3, an enzyme that mediates DNA demethylation, in NKX2-1-negative tumors. Deletion of Foxa1/2 results in loss of TET3 occupancy at key gastric marker genes, indicating that FoxA1/2 recruit TET3 to lineage-specific sites. H3K27ac ChIP-seq and HiChIP show that FoxA1/2 also control the activity of enhancers and promoters as well as their 3D interactions at gastric target genes following NKX2-1 loss. Furthermore, oncogenic KRAS is required for the FoxA1/2-dependent epigenetic reprogramming in NKX2-1-negative LUAD. This work demonstrates the role of FoxA1/2 in rewiring the methylation and histone landscape and cis-regulatory dynamics of NKX2-1-negative LUAD to drive cancer cell lineage switching.

2024-09-11 | GSE247854 | GEO

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [Bisulfite-Seq]

2024-09-11 | GSE247853 | GEO

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [ChIP-seq]

2024-09-11 | GSE247851 | GEO

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [RNA-Seq]

2024-09-11 | GSE247845 | GEO

FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma.

Project description: Not available

| S-EPMC11794038 | biostudies-literature

Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output in Prostate Cancer

Project description:Activation of the androgen receptor (AR) is the key lineage-specific oncogenic pathway and the primary therapeutic target in prostate cancer. While AR signaling is enabled by the pioneer transcription factor FOXA1, its homolog FOXA2 is specifically expressed in advanced lineage plasticity prostate cancers that have lost the AR signaling axis. However, their roles and utility as drug targets remain incompletely characterized. Here, we show an unexpected collaboration of FOXA1 and FOXA2 in mediating AR-independent cell proliferation in different lineage plasticity cancer subtypes. Conversely, joint loss-of-function or pharmacologic disruption of FOXA1 and FOXA2 leads to the collapse of lineage-specific oncogenic transcription factors followed by cell cycle arrest. In summary, our findings uncover a druggable dependency for AR-positive and -negative prostate cancers.

2026-01-27 | PXD057803 | Pride

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