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CSMD3 loss drives aggressive behavior and tumor consolidation in oral squamous premalignant cells

GSE342871 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/08/06 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
9 samples: 3 × CSMD3, KO guide 1, vs 3 × CSMD3, KO guide 2, vs 3 × WT Control,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)
Oral squamous cell carcinoma (OSCC) remains a significant global health burden. Genomic data identify Csmd3 as the third most frequently mutated gene in HNSCC (29% of cases) correlating with poor clinical outcome and prognosis. Despite this, the functional role of CSMD3 in oral premalignancy and malignant transformation remains largely unexplored.
Read the full summary ↓
In this study, we utilized CRISPR-Cas9 system to inactivate CSMD3 in an oral premalignant cell line and characterize knockout in in vitro oral premalignant cell line and in vivo orthotopic model. Functional assays demonstrate that CSMD3 loss significantly enhances cell survival (P < 0.001), while decreasing migration (P = 0.005). Transcriptomic profiling and Gene Set Enrichment Analysis (GSEA) revealed multi-faceted reprogramming characterized by enriched expression of oncogenic survival and stress signaling genes, metabolic rewiring, inflammatory mediators, and structural remodeling driven by altered expression of contraction, actin cross-linking proteins, and polymerization genes. Orthotopic modeling further revealed that CSMD3 loss resulted in significantly increased tumor area fraction (P < 0.0001) and intratumoral cellular density (P < 0.0001). Our study emphasizes the role of CSMD3 loss in promoting aggressive behavior of oral premalignancy, which has a potential for risk stratification, a novel prognostic or diagnostic biomarker, and a target for therapeutic intervention.
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 GSE342871_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 PRJNA1508999 and SRA study SRP725015. Searching any of these in the dataset finder brings you back here.

Study design
3 × CSMD3, KO guide 1, vs 3 × CSMD3, KO guide 2, vs 3 × WT Control,

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
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