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Nuclear PTK7 Interacts with DNA-PK Drives DNA Repair and Immune Evasion in Triple-negative Breast Cancer

GSE302992 Homo sapiens (human) RNA-seq (gene expression) 9 samples Submitted 2026/07/01 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 9 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
Breast cancerThis series is part of our curated briefing on it.
Samples
9 samples: 3 × PTK7NC, vs 3 × PTK7KO1, vs 3 × PTK7KO2,Groups 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)
Membrane proteins with nuclear localization often exert context-dependent functions, yet the mechanistic understanding of this phenomenon remains limited. PTK7, an evolutionarily conserved pseudokinase and a clinically relevant diagnostic and therapeutic target, has been detected in both membrane and nuclear compartments, but its nuclear function has not been elucidated.
Read the full summary ↓
Here, we identify a critical role of nuclear PTK7 in coordinating DNA damage repair and regulating tumor immunogenicity in triple-negative breast cancer (TNBC). Mechanistically, PTK7 interacts with DNA-PKcs to promote its activation and facilitate non-homologous end-joining (NHEJ). Loss of PTK7 impairs DNA repair and activates type I interferon signaling via cytosolic DNA accumulation, enhancing tumor immunogenicity. These effects are consistent across cellular and mouse tumors, and further validated in patient samples. Clinically, PTK7 expression inversely correlates with tumor-intrinsic immune activation across multiple TNBC cohorts. Collectively, our findings uncover a previously unrecognized nuclear function of PTK7 in modulating DNA repair and immune evasion, and nominate PTK7 as a potential therapeutic target for precision immuno-oncology in TNBC.
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 GSE302992_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 PRJNA1293315 and SRA study SRP601769. Searching any of these in the dataset finder brings you back here.

Study design
3 × PTK7NC, vs 3 × PTK7KO1, vs 3 × PTK7KO2,

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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 Breast cancer 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.