GEO series

Menin-RelA complex antagonizes cancer cell-intrinsic and tumor microenvironment-induced NF-κB hyperactivation to suppress pancreatic neuroendocrine tumorigenesis

GSE329027 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/07/11 Platform GPL34284

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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)
Samples: 12 samples: 6 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)

Pancreatic neuroendocrine tumors (PNETs) are rare neuroendocrine cancers with high mortality rates and an immense unmet medical need. While the genetic and immune landscape of PNETs is defined, the molecular mechanisms linking these factors to tumorigenesis remain poorly understood. Here, we identify NF-κB signaling as a key effector pathway that contributes to PNET tumorigenesis, regulated through both cancer cell extrinsic and intrinsic mechanisms.

Read the full summary ↓

CellChat analysis identifies M2-like macrophages as the dominant source of NF-κB-activating cytokines, and co-culture of PNET cancer cells with THP-1-derived M2-macrophages significantly enhances RelA phosphorylation and colony-forming capacity in vitro. Concurrently, we uncovered a cancer cell intrinsic safeguard mechanism wherein the tumor suppressor menin physically associates with RelA to suppress PNET growth in vitro and in vivo. Molecular docking identified key residues mediating the menin-RelA interaction and revealed three clinically relevant menin mutants (P320R, R415P, W423R) that destabilize this complex, compromising menin’s ability to restrain PNET growth. Mechanistically, menin and RelA co-bind κB sites on promoters of proliferation-associated NF-κB target genes, including NR4A1, and epigenetically silence their expression through reduced H3K27ac. Crucially, NR4A1 depletion or small-molecule inhibition suppresses PNET growth in vitro and in vivo. Together, our findings reveal a novel menin-RelA-NR4A1 axis that regulates PNET growth and demonstrates how extrinsic and intrinsic factors converge on NF-κB signaling, highlighting potential therapeutic avenues.

This dataset

Open GSE329027 in finder → Find more human 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 GSE329027_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 PRJNA1457414 and SRA study SRP694537. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

6 conditions, mostly in duplicate

QGP-1 Empty vector input ×2 QGP-1 pCDH MEN1 input ×2 QGP-1 Empty vector ChIP RelA ×2 QGP-1 MEN1 ChIP RelA ×2 QGP-1 Empty vector ChIP H3K27Ac ×2 QGP-1 MEN1 ChIP H3K27Ac ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 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

GSM9695995 QGP-1 Empty vector input rep 1 QGP-1 Empty vector input
GSM9695996 QGP-1 Empty vector input rep 2 QGP-1 Empty vector input
GSM9695997 QGP-1 pCDH MEN1 input rep 1 QGP-1 pCDH MEN1 input
GSM9695998 QGP-1 pCDH MEN1 input rep 2 QGP-1 pCDH MEN1 input
GSM9695999 QGP-1 Empty vector ChIP RelA rep 1 QGP-1 Empty vector ChIP…
GSM9696000 QGP-1 Empty vector ChIP RelA rep 2 QGP-1 Empty vector ChIP…
GSM9696001 QGP-1 MEN1 ChIP RelA rep 1 QGP-1 MEN1 ChIP RelA
GSM9696002 QGP-1 MEN1 ChIP RelA rep 2 QGP-1 MEN1 ChIP RelA
GSM9696003 QGP-1 Empty vector ChIP H3K27Ac rep 1 QGP-1 Empty vector ChIP…
GSM9696004 QGP-1 Empty vector ChIP H3K27Ac rep 2 QGP-1 Empty vector ChIP…
GSM9696005 QGP-1 MEN1 ChIP H3K27Ac rep 1 QGP-1 MEN1 ChIP H3K27Ac
GSM9696006 QGP-1 MEN1 ChIP H3K27Ac rep 2 QGP-1 MEN1 ChIP H3K27Ac

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