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Lethal giant larvae gene family functions as a tumor suppressor in skin epidermis

GSE247772 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/11/13 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × Control vs 3 × L1L2cKO vs 3 × L1L2p53cKO vs 3 × p53cKOGroups 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)
Loss of cell polarity and tissue disorganization occurs in majority of epithelial tumors. The role of cell polarity mechanisms in cancer is not completely understood. Here we analyzed the mammalian orthologs of drosophila apical-basal polarity gene lethal giant larvae (lgl), which also functions as a tumor suppressor in flies. There are two mammalian orthologs of lgl (Llgl1 and Llgl2).
Read the full summary ↓
To determine the role of the entire Lgl signaling pathway in mammals we generated mice with ablation of both Llgl1 and Llgl2 in skin epidermis (Llgl1/2-/- cKO mice). Surprisingly, we found that ablation of Llgl1/2 does not impact epidermal polarity. However, old Llgl1/2-/- cKO mice develop skin lesions which are missing epidermal layer and ripe with inflammation. To determine the role of Llgl1/2 in cancer we generated Trp53-/-/Llgl1/2-/- and Trp53-/+/Llgl1/2-/- cKO mice. Loss of Llgl1/2 promoted squamous cell carcinoma (SCC) development in Trp53-/- cKO and caused SCC in Trp53-/+ cKO mice, while no cancer was observed in Trp53-/+ cKO controls. Mechanistically, we show that ablation of Llgl1/2 activates aPKC-NF-B-RelA signaling pathway and epidermis-specific deletion of only one allele of RelA rescues SCC phenotype in Trp53-/+/Llgl1/2-/- cKO mice. We conclude that Lgl signaling pathway functions as a tumor suppressor in mammalian skin.
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 GSE247772_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 PRJNA1040296 and SRA study SRP471886. Searching any of these in the dataset finder brings you back here.

Study design
3 × Control vs 3 × L1L2cKO vs 3 × L1L2p53cKO vs 3 × p53cKO

Supports a between-group comparison across 12 samples.

How we read this: 4 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.