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Atovaquone-induced oxidative stress activates pentose phosphate pathway and immunogenic cell death in ovarian cancer

GSE288243 Homo sapiens (human) RNA-seq (gene expression) 39 samples Submitted 2025/02/02 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 39 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Topic
Ovarian cancerThis series is part of our curated briefing on it.
Samples
39 samples: 12 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.
Paper
Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancerScientific reports · 2025
Summary (written by the submitters)
Atovaquone, an FDA-approved oxidative phosphorylation (OXPHOS) inhibitor, has shown promise in treating epithelial ovarian cancer (EOC), the deadliest gynecologic malignancy. However, the precise mechanisms underlying its antitumorigenic effects remain unclear. We employed a longitudinal transcriptomic approach to characterize the molecular effects of atovaquone on EOC cells.
Read the full summary ↓
Our findings demonstrate that atovaquone disrupts cellular homeostasis and metabolism, activates stress responses, and primes immune recognition. We observed temporal downregulation of genes and pathways involved in key cellular processes, such as cell cycle and DNA replication, correlating with reduced proliferative capacity. Atovaquone also downregulated both OXPHOS and glycolysis, while upregulating the pentose phosphate pathway, suggesting a metabolic shift toward redox homeostasis restoration in response to severe oxidative stress. Consistent with oxidative stress, we found that atovaquone activated endoplasmic reticulum (ER) stress, which is linked to immunogenic cell death. During ER stress, calreticulin, a Damage-Associated Molecular Pattern (DAMP), translocates to the plasma membrane, where it promotes immune recognition. We observed that calreticulin was upregulated on the plasma membrane of atovaquone-treated EOC cells. Additionally, we detected increased levels of other DAMPs, such as High Mobility Group Box 1 (HMGB1) and Mitochondrial Transcription Factor A (TFAM), in the supernatant of atovaquone-treated cells, indicating the release of immunogenic molecules. Moreover, increased expression of ligands for activating receptors of NK cells was observed and co-culture experiments showed enhanced NK cell activity toward atovaquone-treated cells. These results highlight atovaquone’s potential as an adjuvant therapy that activates immune responses, offering a new avenue for combination therapies in EOC treatment.
Published in
Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancer
Betancourt Ponce M, Boonpattrawong N, Fagan AJ et al. · Scientific reports 2025 · PMID 41286323 · doi:10.1038/s41598-025-25704-y
This dataset
Open GSE288243 in finder → Find more human RNA-seq datasets → Ovarian 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 GSE288243_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1216615 and SRA study SRP560407. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41286323) ↗
Study design
12 conditions, mostly in duplicate
OVCAR3 cells, DMSO treated, 48 hours, batch C, ×3 OVCAR3 cells, 30μM Atovaquone treated, 48 hou… ×3 OVCAR3 cells, 45μM Atovaquone treated, 48 hou… ×3 OVCAR3 cells, DMSO treated, 1 hour, batch B, ×2 OVCAR3 cells, 30μM Atovaquone treated, 1 hour… ×2 OVCAR3 cells, 45μM Atovaquone treated, 1 hour… ×2 OVCAR3 cells, DMSO treated, 8 hours, batch B, ×2 OVCAR3 cells, 30μM Atovaquone treated, 8 hour… ×2 +16 more

Supports a between-group comparison across 27 samples.

How we read this: 12 replicated groups read from 39 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 Ovarian cancer datasets

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