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Targeting COPA to enhance erdafitinib sensitivity in FGFR-altered bladder cancer

GSE278672 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/05/22 Platform GPL24676
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
Bladder cancerThis series is part of our curated briefing on it.
Samples
12 samples: 12 samples, each with a distinct title — no replicated groupsGroups 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
Targeting COPA to Enhance Erdafitinib Sensitivity in FGFR-Altered Bladder CancerAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
Summary (written by the submitters)
Fibroblast growth factor receptor (FGFR) family aberrations are common in urothelial cancer. The FGFR tyrosine kinase inhibitor erdafitinib has been approved for locally advanced or metastatic urothelial cancer with FGFR2/3 alterations. Despite the initial efficacy of erdafitinib, resistance cannot be avoided. The molecular mechanism of erdafitinib resistance has not been well investigated.
Read the full summary ↓
Here, we performed genome-wide CRISPR screen and identified coatomer protein complex subunit α (COPA) as a key target to enhance erdafitinib sensitivity. Functionally, the deficiency of COPA reduced the proliferation of FGFR-altered bladder cancer cells upon erdafitinib treatment. Mechanistically, COPA knockout increased LRPPRC protein degradation, leading to reduced ID3 mRNA stability in an m6A-dependent manner. Collectively, these findings reveal a novel mechanism of erdafitinib resistance, providing a potential therapeutic target for FGFR-altered bladder cancer.
Published in
Targeting COPA to Enhance Erdafitinib Sensitivity in FGFR-Altered Bladder Cancer
Zhao H, Gao X, Jiang Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2025 · PMID 40112217 · doi:10.1002/advs.202413209
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 GSE278672_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 PRJNA1168176 and SRA study SRP536310. Searching any of these in the dataset finder brings you back here.

Study design
12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 distinct titles with little repetition. 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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