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Investigating therapy-induced senescence as a reversible escape mechanism of drug resistance in breast cancer cells using high-dose doxorubicin treatment

GSE280381 Homo sapiens (human) Single-cell RNA-seq 12 samples Submitted 2025/05/07 Platform GPL24676
At a glance

Single-cell RNA-seq · human · 12 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Homo sapiens (human)
Samples
12 samples: 6 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
Therapy-induced senescence is a transient drug resistance mechanism in breast cancerMolecular cancer · 2025
Summary (written by the submitters)
The emergence of drug resistance remains a critical challenge in cancer treatment, significantly contributing to high mortality rates. Here, we investigate therapy-induced senescence (TIS) as a reversible escape mechanism of drug resistance in breast cancer cells. Using high-dose doxorubicin, we induced TIS in MCF7 and T47D breast cancer cell lines.
Read the full summary ↓
scRNA sequencing revealed a unique transcriptomic profile for TIS cells, distinct from both parental and repopulated cells in every cell line, exposing a small subpopulation of TIS cells with the potential to escape senescence. Gene set enrichment analysis indicated significant downregulation of proliferation-related genes, downregulation of DNA repair pathways, and the upregulation of immune response related genes.
Published in
Therapy-induced senescence is a transient drug resistance mechanism in breast cancer
Bajtai E, Kiss C, Bakos É et al. · Molecular cancer 2025 · PMID 40312750 · doi:10.1186/s12943-025-02310-0
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 GSE280381_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1178141 and SRA study SRP541015. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
MCF7, CTR, ×2 MCF7, TIS, ×2 MCF7, REPOP, ×2 T47D, CTR, ×2 T47D, TIS, ×2 T47D, REPOP, ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 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
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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.