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

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

PROVIDER: PRJNA1040822 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26842102_1.fastq.gz	Fastqsanger.gz
	SRR26842102_2.fastq.gz	Fastqsanger.gz
	SRR26842103_1.fastq.gz	Fastqsanger.gz
	SRR26842103_2.fastq.gz	Fastqsanger.gz
	SRR26842104_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 [Bisulfite-Seq]

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 | GSE247853 | GEO

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]

| PRJNA1040823 | 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 [RNA-Seq]

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

| PRJNA1040817 | ENA

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

2024-09-11 | GSE247854 | 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

Epigenomic analyses of FOXA1-mediated enhancer reprogramming to control tumor subtype plasticity through HH-BMP-FOXA1 signalling feedback between urothelial tumor and stromal fibroblasts [FOXA1 ChIP-seq]

Project description:Consistent with the previous study, we showed that tumor molecular subtypes switched between the luminal subtype and the basal subtype during long-term maintenance of conventional tumor organoids in the absence of stroma in vitro, indicating the important role of tumor stroma in maintaining the tumor phenotype. Interestingly, genomic alterations seen in parental tumors are preserved well in both conventional tumor organoids and tumor assembloids, implying that the determination of tumor phenotypes may rely on epigenetic changes in tumor stroma-dependent ways, particularly through stromal BMP signals, elicited by Hh expression in tumor cells. We performed extensive epigenomic analyses including RNA-seq, ATAC-seq, and ChIP-seq with genetically manipulated tumor assembloids, in which genetic manipulations were applied independently to tumor organoids and tumor stroma in a combinatorial manner. Using this system, we identified FOXA1 as a master pioneering factor that drives enhancer reprogramming during the molecular switching of tumor subtypes. We have also obtained new evidence that FOXA1 is induced by stromal BMP signals and identified the HH-BMP-FOXA1 signaling feedback between urothelial tumors and stromal fibroblasts as a critical signaling axis in the FOXA1-mediated enhancer reprogramming of tumor phenotypes in the determination of urothelial carcinomas.

2020-09-27 | GSE141354 | GEO

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