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MYB and HIF1α crosstalk drives hypoxia-induced transcriptional reprogramming and adaptive signaling alterations in pancreatic cancer [ChIP-seq]

GSE292665 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 27 samples Submitted 2025/07/17 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 27 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
Homo sapiens (human)
Topic
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
27 samples: 9 conditions, mostly in triplicateGroups 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.
Paper
MYB and HIF1α crosstalk drives hypoxia-induced transcriptional reprogramming and adaptive signaling alterations in pancreatic cancerCancer letters · 2025
Summary (written by the submitters)
Pancreatic cancer is an aggressive malignancy, characterized by extensive desmoplasia and a hypoxic tumor microenvironment that contributes to therapy resistance. MYB, a proto-oncogene encoding a transcription factor, plays a crucial role in pancreatic tumor growth, metastasis, and desmoplasia. Recently, we also revealed a role of MYB in hypoxic survival of pancreatic cancer by promoting metabolic reprogramming through interaction with HIF1α, modulating its expression and influencing its binding to glycolytic gene promoters.
Read the full summary ↓
In this study, we examined the impact of hypoxia on the genome-wide occupancy of MYB by performing chromatin immunoprecipitation sequencing (ChIP-seq) analysis. We also used HIF1A knockout cells to investigate the role of HIF1α in altered genomic occupancy of MYB. In addition, we examined the genomic distribution of HIF1α in presence and absence of MYB and the impact of their crosstalk on transcriptional reprogramming and associated signaling alterations by RNA-seq and pathway analyses. Our findings show that hypoxia induces significant changes in MYB’s genomic distribution, partially dependent on HIF1α, and that MYB facilitates HIF1α binding to specific gene promoters. We also identify a subset of hypoxia-induced genes co-regulated by MYB and HIF1α, involved in oncogenic signaling pathways critical for hypoxic adaptation. These results highlight the reciprocal crosstalk between MYB and HIF1α, providing novel mechanistic insights into pancreatic cancer adaptation under hypoxia and suggesting MYB as a potential therapeutic target.
Published in
MYB and HIF1α crosstalk drives hypoxia-induced transcriptional reprogramming and adaptive signaling alterations in pancreatic cancer
Anand S, Vikramdeo KS, Khan MA et al. · Cancer letters 2025 · PMID 40680814 · doi:10.1016/j.canlet.2025.217916
This dataset
Open GSE292665 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Pancreatic cancer landscape →
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 GSE292665_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 PRJNA1240653 and SRA study SRP572365. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40680814) ↗
Study design
9 conditions, mostly in triplicate
ChIP-seq, MYB, Normoxia, MiaPaCa-2 cells, ×3 Input, Normoxia, MiaPaCa-2 cells, ×3 ChIP-seq, MYB, Hypoxia, MiaPaCa-2 cells, ×3 Input, Hypoxia, MiaPaCa-2 cells, ×3 ChIP-seq, MYB, Hypoxia, MiaPaCa-HIF1α KO, ×3 Input, Hypoxia, MiaPaCa-HIF1α KO, ×3 ChIP-seq, HIF1α, Hypoxia, MiaPaCa-2 cells, ×3 ChIP-seq, HIF1α, Hypoxia, MiaPaCa-MYB KO-HIF1… ×3 +1 more

Supports a between-group comparison across 27 samples.

How we read this: 9 replicated groups read from 27 sample titles; they account for 27 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
More Pancreatic cancer datasets

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.