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Pygo2 Loss Induces Tertiary Lymphoid Structure Formation and Enhances Immunotherapy and Castration Responses in Prostate Cancer

GSE315303 Mus musculus (mouse) RNA-seq (gene expression) 22 samples Submitted 2026/06/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 22 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
Mus musculus (mouse)
Samples
22 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.
Summary (written by the submitters)
Prostate cancer (PCa) is widely regarded as an immunologically "cold" tumor, and the presence and regulation of tertiary lymphoid structures (TLSs) in it remain poorly understood. Using a prostate-specific Pten/Smad4 knockout (DKO) model, we found that additional deletion of Pygo2 (TKO) markedly enhanced TLS formation, increased TLS-associated chemokines and cytokines, and promoted lymphocyte organization within the tumor microenvironment.
Read the full summary ↓
Pygo2 loss also restored androgen receptor (AR) signaling and sensitized tumors to castration. Importantly, combination therapy with castration, CXCR2 inhibition, and immune checkpoint blockade (CSI) further matured TLSs, strengthened B and T cell responses, and induced durable disease control in >80% of TKO mice for more than 42 weeks. Mechanistically, Pygo2 deletion led to DNA damage accumulation and activation of the STING-interferon pathway, whereas STING silencing abolished this response. Collectively, these findings identify Pygo2 as a key regulator of TLS formation, immune activation, and therapy resistance, highlighting it as a promising therapeutic target in castration-resistant prostate cancer.
This dataset
Open GSE315303 in finder → Find more mouse RNA-seq datasets →
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 GSE315303_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 PRJNA1344337. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
6 conditions, mostly in duplicate
Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L, tumor, c… ×3 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L Pygo2-L/L… ×3 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L, tumor, u… ×2 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L Pygo2-L/L… ×2 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L single-ce… ×2 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L Pygo2-L/L… ×2 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L Pygo2-L/L… ×1 Nkx3.1-CreERT2/+ Pten-L/L Smad4-L/L Pygo2-L/L… ×1 +6 more

Supports a between-group comparison across 14 samples.

How we read this: 6 replicated groups read from 22 sample titles; they account for 14 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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