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The Acetyltransferase ARD1 Induces Glutathione Synthesis to Facilitate Ferroptosis Evasion in Hepatocellular Carcinoma

GSE301304 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/08/02 Platform GPL16791
At a glance

RNA-seq (gene expression) · human · 12 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
Hepatocellular carcinomaThis series is part of our curated briefing on it.
Samples
12 samples: 3 × 3B-NC vs 3 × 3B-Si vs 3 × H7-NC vs 3 × H7-SiGroups 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
The Acetyltransferase ARD1 Induces Glutathione Synthesis to Facilitate Ferroptosis Evasion in Hepatocellular CarcinomaCancer research · 2025
Summary (written by the submitters)
Aberrant upregulation of the intracellular antioxidant glutathione (GSH) is implicated in promoting tumor proliferation, inducing drug resistance, and inhibiting ferroptosis across various malignancies, including hepatocellular carcinoma (HCC). Targeting the mechanism underlying GSH upregulation in HCC could represent a therapeutic strategy to improve patient outcomes.
Read the full summary ↓
In this study, we employed a genome-wide CRISPR‒Cas9 screen and targeted metabolomics to identify the acetyltransferase ARD1 as a pivotal facilitator of de novo GSH synthesis in HCC. Notably, ARD1 upregulation was positively correlated with elevated GSH levels and poor prognosis in HCC patients. In vivo and in vitro functional assays revealed that ARD1 promoted HCC cell proliferation and inhibited ferroptosis in a GSH-dependent manner. LC‒MS/MS-based stable isotope labeling revealed that ARD1 increased GSH levels by stabilizing γ-glutamylcysteine ligase catalytic subunit (GCLC) mRNA, which was mediated by the RNA-binding protein PABPC1. Mechanistically, ARD1 acetylated PABPC1 at K167, augmenting its cytoplasmic retention by disrupting PABPC1-importin α7 complex formation. Cytoplasmic PABPC1 then interacted with eIF4G to collaboratively stabilize GCLC mRNA, preventing its degradation, increasing GSH synthesis, and ultimately conferring ferroptosis resistance in HCC cells. Furthermore, oxidative stress induced by hydrogen peroxide suppressed ARD1 ubiquitination and degradation, thereby promoting PABPC1 cytoplasmic translocation and inducing GCLC expression. ARD1 suppression promoted sorafenib-mediated ferroptosis in HCC patient-derived xenograft tumors with high ARD1 and GCLC expression. Overall, this research uncovers an oxidative stress–ARD1–PABPC1–GCLC axis with a crucial role in GSH metabolic reprogramming and ferroptosis regulation in HCC and reveals a strategy for ferroptosis-based targeted therapy for HCC.
Published in
The Acetyltransferase ARD1 Induces Glutathione Synthesis to Facilitate Ferroptosis Evasion in Hepatocellular Carcinoma
Liu Y, Liu F, Liu J et al. · Cancer research 2025 · PMID 40838989 · doi:10.1158/0008-5472.CAN-24-4015
This dataset
Open GSE301304 in finder → Find more human RNA-seq datasets → Hepatocellular carcinoma 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 GSE301304_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 PRJNA1284777 and SRA study SRP596383. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40838989) ↗
Study design
3 × 3B-NC vs 3 × 3B-Si vs 3 × H7-NC vs 3 × H7-Si

Supports a between-group comparison across 12 samples.

How we read this: 4 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
More Hepatocellular carcinoma datasets

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