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Cannabinoid-driven epigenetic remodeling of a chromatin-lipid homeostatic axis via ARID1A uncovers a metabolic vulnerability in cancer

GSE309010 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 25 samples Submitted 2026/07/27 Platform GPL21697Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 25 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
25 samples: 8 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.
Summary (written by the submitters)
A substantial body of evidence supports a tumor suppressor role for the chromatin remodeler ARID1A, whose inactivating mutations and loss of function are common across human cancers. These alterations have spurred extensive efforts to uncover vulnerabilities associated with ARID1A deficiency. However, emerging studies suggest that ARID1A may also exert context-dependent tumor-promoting functions, opening new therapeutic avenues in ARID1A-proficient tumors.
Read the full summary ↓
In endometrial cancer (EC), ARID1A mutations typically arise late during tumor progression and are dispensable for tumor initiation, providing a relevant context to interrogate its noncanonical homeostatic roles. Here, through integrated multiomics analyses, cellular bioenergetics and in vivo studies using EC patient-derived xenografts and genetically engineered mouse models, we demonstrate that functional ARID1A is required for acquired resistance to nutrient deprivation induced by antiangiogenic (starvation) therapy. Mechanistically, ARID1A orchestrates an epigenetically regulated chromatin-lipid homeostatic program involving lipid metabolism and mitochondrial fatty acid oxidation. Unexpectedly, we find that Δ9- tetrahydrocannabinol (THC), a phytocannabinoid and orthosteric CB1/CB2 agonist, exerts its antitumor activity by repressing ARID1A, thereby dismantling this chromatin- lipid metabolic axis and restoring sensitivity to starvation therapy. These findings position ARID1A as a central node linking chromatin remodeling to metabolic plasticity, and identify THC as a pharmacologic disruptor of this epigenetic metabolic program with therapeutic potential in ARID1A-proficient tumors.
This dataset
Open GSE309010 in finder → Find more human RNA-seq 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 GSE309010_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 PRJNA1333710 and SRA study SRP626263. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
8 conditions, mostly in triplicate
HEC-1A UNTREATED Biol ×3 HEC-1A THC 20uM 24h Biol ×3 HEC-1A THC 20uM 72h Biol ×3 HEC-1A, THC 20uM, 24h, ATAC-seq, Biol ×3 HEC-1A, THC 20uM, 72h, ATAC-seq, Biol ×3 HEC-1A, UNTREATED, ATAC-seq, Biol ×3 HEC-1A, UNTREATED, H3K4me3 (CUT&RUN), Biol ×3 HEC-1A, THC 20uM, H3K4me3 (CUT&RUN), Biol ×3 +1 more

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 25 sample titles; they account for 24 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
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