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Transient CB2R Modulation Promotes Luminal-like Differentiation and Restricts Breast Cancer Plasticity

GSE333169 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/07/30 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 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
Mus musculus (mouse)
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)
Cancer cell plasticity enables therapy resistance and metastasis by allowing transitions between stem-like and differentiated states. Differentiation-based strategies aim to stabilize tumor cell identity, yet pharmacological approaches that induce durable lineage restriction remain limited. Here, we show that transient modulation of cannabinoid receptor 2 (CB2R) promotes persistent luminal-like stabilization in breast cancer models.
Read the full summary ↓
Using patient-derived and murine tumor organoids, we demonstrate that brief, low-dose CB2R modulation reduces self-renewal, invasiveness and tumor-initiating capacity, while enhancing tamoxifen sensitivity and limiting the emergence of resistant phenotypes. These effects persist under pro-dedifferentiation conditions, including TGFb exposure, stromal co-culture, immune signaling and mechanical stress, and are long-term maintained in vivo following orthotopic transplantation. RNAseq analyses reveal a trajectory from an early plastic state toward a stabilized luminal-like identity, supported by CUT&Tag profiling that uncovers chromatin remodeling in this transition. Together, our findings redefine CB2R as a regulator of tumor cell state rather than solely a mediator of cytotoxic responses and establish transient CB2R modulation as a strategy to durably constrain breast cancer plasticity through differentiation-based therapy.
This dataset
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.

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 GSE333169_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1470239 and SRA study SRP703453. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
H3K4me3 coverage on control -treated spheroid… ×2 H3K4me3 coverage on SR2 -treated spheroids at… ×2 H3K4me3 coverage on THC -treated spheroids at… ×2 H3K27me3 coverage on control -treated spheroi… ×2 H3K27me3 coverage on SR2 -treated spheroids a… ×2 H3K27me3 coverage on THC -treated spheroids a… ×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
Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag datasets in GEO →

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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.