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Prostate-specific CRISPR knock-in of human SKP2 induces prostatic intraepithelial neoplasia and adenocarcinoma and reprograms prostate microenvironment.

GSE295398 Mus musculus (mouse) Single-cell RNA-seq 8 samples Submitted 2026/07/24 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 8 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
Mus musculus (mouse)
Samples
8 samples
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)
S-phase kinase associated protein 2 (SKP2), an oncogene and promising therapeutic target, required for spontaneous tumor development in the retinoblastoma protein (pRB), PTEN or p53 deficient mice. We therefore have established a prostate specific CRISPR human SKP2 (hSKP2) knock-in mouse model for studying its role in prostate carcinogenesis.
Read the full summary ↓
Overexpression of hSKP2 which is driven by endogenous mouse probasin promoter induces prostatic lesions including hyperplasia, mouse prostate intraepithelial neoplasia (mPIN), and low-grade carcinoma and increase prostate weights. Transcriptional profiling by RNA-sequencing analysis revealed significant gene expression alterations in epithelial to mesenchymal transition (EMT), extracellular matrix and interferon signaling in the prostate of hSKP2 knock-in mice compared to wild-type mice. Single cell deconvolution showed an increase of fibroblasts population and a decrease of CD8+T cell and B cell populations in the prostates of hSKP2-knock-in mice. Consistently with these results, overexpression of hSKP2 in human prostate cancer PC3 cells markedly increased cell migration and invasion and induced the gene expression of EMT and interferon pathways, including FMOD, THY1, PFPK, USP18, IL15, etc. In addition, prostate organoids were derived from hSKP2 knock-in and wild -type mouse prostates. Known SKP2 inhibitors Flavokawain A (FKA) and C1 both selectively decrease the viability and alter the morphologies of hSKP2 knock-in versus wild-type prostate organoids. Our studies have provided a new well-characterized prostate-specific hSKP2 knock-in mouse model for testing novel SKP2 targeting agents and new mechanistic insights for understanding an oncogenic role of SKP2 on prostate microenvironment.
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 GSE295398_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 PRJNA1254599 and SRA study SRP580738. Searching any of these in the dataset finder brings you back here.

Samples in this study

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