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Identification of potential targets of FTO in GIST via transcriptome-wide RNA-seq

GSE240411 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2026/06/10 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 24 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
Gastrointestinal stromal tumourThis series is part of our curated briefing on it.
Samples
24 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)
Tyrosine kinase inhibitor (TKIs) resistance remains the leading obstacle for treating gastrointestinal stromal tumor (GIST), in which the secondary mutations within KIT causes escape of TKI inhibition and KIT reactivation. Here we found FTO was highly expressed in GIST and positively correlated with the high-grade and recurrence liability.
Read the full summary ↓
m6A-seq and RNA-seq analyses of GIST cells treated with FTO inhibitor CS1 demonstrated that FTO demethylated the m6A modification in the 3’UTR of KIT mRNA, which in turn partially blocked recognition by m6A reader YTHDF2, thus enhanced KIT mRNA stability. Pharmacological inhibition or genetic knockdown of FTO led to decreased KIT expression, mitigated malignant phenotypes and increased imatinib sensitivity in vitro, while genetic knockout of FTO or entacapone treatment combined with imatinib evoked regression of tumor in KIT-Asp818Tyr/+ heterozygote GIST mouse model. Phase I trial in five TKIs-refractory GIST patients with a combination of entacapone and imatinib (NCT 04006769) demonstrated that two of three assessable participants (66.7%) achieved partial remission. Our results suggest that targeting FTO is a feasible therapeutic strategy for clinical management of TKI resistance and recurrence of GIST.
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 GSE240411_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: 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 PRJNA1003533 and SRA study SRP454095. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in triplicate
GIST-48 cells, CS1 ×3 GIST-48 cells, DMSO ×3 GIST-430 cells, CS1 ×3 GIST-430 cells, DMSO ×3 GIST-T1 cells, CS1 ×3 GIST-T1 cells, DMSO ×3 GIST-882 cells, CS1 ×3 GIST-882 cells, DMSO ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 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
More Gastrointestinal stromal tumour datasets

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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.