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Targeting MYC effector functions in pancreatic cancer by inhibiting the ATPase RUVBL1/2

GSE216095 synthetic construct; Mus musculus ChIP-seq / ATAC-seq (genome binding and open chromatin) 87 samples Submitted 2024/06/01 Platform GPL19424Platform GPL30172Platform GPL19057
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · synthetic construct; Mus musculus · 87 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
synthetic construct; Mus musculus
Samples
87 samples: 21 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
Targeting MYC effector functions in pancreatic cancer by inhibiting the ATPase RUVBL1/2Gut · 2024
Summary (written by the submitters)
Objective: The hallmark oncogene MYC drives the progression of most tumorstumours, but direct inhibition of MYC by a small-molecule drug has not reached clinical testing. MYC is a transcription factor that depends on several binding partners to function. We therefore explored the possibility of targeting MYC via its interactome in pancreatic ductal adenocarcinoma (PDAC).
Read the full summary ↓
Design: To identify the most suitable targets among all MYC binding partners, we constructed a targeted shRNA library and performed screens in cultured PDAC cells and tumorstumours in mice.Results:Unexpectedly, many MYC binding partners were found to be important for cultured PDAC cells but dispensable in vivo. However, some were also essential for tumorstumours in their natural environment and, among these, the ATPases RUVBL1 and RUVBL2 ranked first. Degradation of RUVBL1 by the auxin-degron system led to the arrest of cultured PDAC cells but not untransformed cells and to complete tumortumour regression in mice, which was preceded by immune cell infiltration. Mechanistically, RUVBL1 was required for MYC to establish oncogenic and immuno-evasive gene expression identifying the RUVBL1/2 complex as a druggable vulnerability in MYC-driven cancer. Conclusion: One implication of our study is that PDAC cell dependencies are strongly influenced by the environment, so genetic screens should be performed in vitro and in vivo. Moreover, the auxin-degron system can be applied in a PDAC model, allowing target validation in living mice. Finally, by revealing the nuclear functions of the RUVBL1/2 complex, our study presents a pharmaceutical strategy to render pancreatic cancers potentially susceptible to immunotherapy.
Published in
Targeting MYC effector functions in pancreatic cancer by inhibiting the ATPase RUVBL1/2
Vogt M, Dudvarski Stankovic N, Cruz Garcia Y et al. · Gut 2024 · PMID 38821858 · doi:10.1136/gutjnl-2023-331519
This dataset
Open GSE216095 in finder → Find more 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 GSE216095_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 PRJNA892074 and SRA study SRP403474. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38821858) ↗
Study design
21 conditions, mostly in triplicate
KPC_allograft_screen_Ctrl ×5 KPC_allograft_screen_Dox ×5 KPC_culture_screen_Ctrl ×3 KPC_culture_screen_Dox ×3 SLAMseq_AID_Ruvbl1_Auxin_3h ×3 SLAMseq_AID_Ruvbl1_Ctrl_15h ×3 SLAMseq_CB6644_MYC_ER_CB6644_OHT ×3 SLAMseq_CB6644_MYC_ER_CB6644 ×3 +34 more

Supports a between-group comparison across 66 samples.

How we read this: 21 replicated groups read from 87 sample titles; they account for 66 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

+ 47 more — browse all 87 samples with per-sample file links →

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