GEO series

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

GSE247851 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 40 samples Submitted 2024/09/11 Platform GPL24247

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 40 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Mus musculus (mouse)
Samples: 40 samples: 20 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

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.

Read the full summary ↓

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.

This dataset

Open GSE247851 in finder → Find more mouse ChIP / ATAC / CUT&Tag datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE247851_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1040816 and SRA study SRP472077. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

20 conditions, mostly in duplicate

KN-FoxA1-Input, ×2 KN-FoxA1, ×2 KN-TET3-Input, ×2 KN-TET3, ×2 KNF1F2-TET3-Input, ×2 KNF1F2-TET3, ×2 KN-H3K27ac-Input, ×2 KN-H3K27ac, ×2 +12 more

Supports a between-group comparison across 40 samples.

How we read this: 20 replicated groups read from 40 sample titles; they account for 40 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM7901533 KN-FoxA1-Input, replicate 1 KN-FoxA1-Input,
GSM7901534 KN-FoxA1, replicate 1 KN-FoxA1,
GSM7901535 KN-FoxA1-Input, replicate 2 KN-FoxA1-Input,
GSM7901536 KN-FoxA1, replicate 2 KN-FoxA1,
GSM7901537 KN-TET3-Input, replicate 1 KN-TET3-Input,
GSM7901538 KN-TET3, replicate 1 KN-TET3,
GSM7901539 KN-TET3-Input, replicate 2 KN-TET3-Input,
GSM7901540 KN-TET3, replicate 2 KN-TET3,
GSM7901541 KNF1F2-TET3-Input, replicate 1 KNF1F2-TET3-Input,
GSM7901542 KNF1F2-TET3, replicate 1 KNF1F2-TET3,
GSM7901543 KNF1F2-TET3-Input, replicate 2 KNF1F2-TET3-Input,
GSM7901544 KNF1F2-TET3, replicate 2 KNF1F2-TET3,
GSM7901545 KN-H3K27ac-Input, replicate 1 KN-H3K27ac-Input,
GSM7901546 KN-H3K27ac, replicate 1 KN-H3K27ac,
GSM7901547 KN-H3K27ac-Input, replicate 2 KN-H3K27ac-Input,
GSM7901548 KN-H3K27ac, replicate 2 KN-H3K27ac,
GSM7901549 KNF1F2-H3K27ac-Input, replicate 1 KNF1F2-H3K27ac-Input,
GSM7901550 KNF1F2-H3K27ac, replicate 1 KNF1F2-H3K27ac,
GSM7901551 KNF1F2-H3K27ac-Input, replicate 2 KNF1F2-H3K27ac-Input,
GSM7901552 KNF1F2-H3K27ac, replicate 2 KNF1F2-H3K27ac,
GSM7901553 22E-FoxA1-Input, replicate 1 22E-FoxA1-Input,
GSM7901554 22E-FoxA1, replicate 1 22E-FoxA1,
GSM7901555 22E-FoxA1-Input, replicate 2 22E-FoxA1-Input,
GSM7901556 22E-FoxA1, replicate 2 22E-FoxA1,
GSM7901557 KG1A-FoxA1-Input, replicate 1 KG1A-FoxA1-Input,
GSM7901558 KG1A-FoxA1, replicate 1 KG1A-FoxA1,
GSM7901559 KG1A-FoxA1-Input, replicate 2 KG1A-FoxA1-Input,
GSM7901560 KG1A-FoxA1, replicate 2 KG1A-FoxA1,
GSM8524573 KN-FoxA2-Input, replicate 1 KN-FoxA2-Input,
GSM8524574 KN-FoxA2, replicate 1 KN-FoxA2,
GSM8524575 KN-FoxA2-Input, replicate 2 KN-FoxA2-Input,
GSM8524576 KN-FoxA2, replicate 2 KN-FoxA2,
GSM8524577 KN-TET2-Input, replicate 1 KN-TET2-Input,
GSM8524578 KN-TET2, replicate 1 KN-TET2,
GSM8524579 KN-TET2-Input, replicate 2 KN-TET2-Input,
GSM8524580 KN-TET2, replicate 2 KN-TET2,
GSM8524581 KNF1F2-TET2-Input, replicate 1 KNF1F2-TET2-Input,
GSM8524582 KNF1F2-TET2, replicate 1 KNF1F2-TET2,
GSM8524583 KNF1F2-TET2-Input, replicate 2 KNF1F2-TET2-Input,
GSM8524584 KNF1F2-TET2, replicate 2 KNF1F2-TET2,

Datasets on a similar topic

GSE247845 FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma [RNA-Seq] 20 samples shares foxa1, adenocarcinoma, reprogramming, 2-dependent, epigenomic, switching, lineage
GSE302859 Multi-tier signaling and epigenomic reprogramming drive microglial inflammatory states and functions associated with demyelination [ChIP-seq] 28 samples shares reprogramming, epigenomic, chip-seq
GSE278100 Foxa1-Mediated Chromatin Remodeling and Enhancer Reprogramming Promotes Gemcitabine Resistance in Pancreatic Cancer 54 samples shares foxa1, reprogramming
GSE302858 Multi-tier signaling and epigenomic reprogramming drive microglial inflammatory states and functions associated with demyelination [ATAC-seq] 42 samples shares reprogramming, epigenomic
GSE306458 ACVR1-mediated glycolytic reprogramming promotes histone lactylation and neuronal pyroptosis in neuropathic pain {ChIP-seq] 12 samples shares reprogramming, chip-seq
GSE268822 Transcriptional landscapes underlying Notch-induced lineage conversion and reprogramming of mammary cells 840 samples shares reprogramming, lineage
GSE302857 Multi-tier signaling and epigenomic reprogramming drive microglial inflammatory states and functions associated with demyelination [RNA-seq] 81 samples shares reprogramming, epigenomic
GSE281941 Klf5 functions as a multi-lineage reprogramming transcription factor 30 samples shares reprogramming, lineage

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