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Transcriptional and UV-response regulatory role of PPARb in Normal Human Keratinocytes

GSE263846 Homo sapiens (human) RNA-seq (gene expression) 48 samples Submitted 2024/12/18 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 48 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)
Samples
48 samples: 16 conditions, mostly in triplicateGroups 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.
Paper
Transcriptional and functional regulation of cell cycle and UV response by PPARβ in human skin epidermal cellsFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
Summary (written by the submitters)
Solar radiation is the major source of human exposure to UV radiation, the major carcinogen in skin cancers, by triggering a number of cellular responses that can indirectly or directly induce DNA damage. Skin cells attempt to repair these damages by activating cascades of DNA Damage Response mechanisms to safeguard genome integrity, thereby preventing skin cancers.
Read the full summary ↓
The role of PPARb - a druggable transcription factor, in the development of UV-dependent skin cancers is not mechanistically elucidated. We have shown previously that PPARb knockout mice are less prone to UV-induced skin cancers. Here, we report on our global transcriptomic analysis revealing that PPARb directly regulates gene expression programs associated with cell cycle and DNA repair pathways in normal human epidermal keratinocytes. We show that in these cells, as well as in malignant human keratinocytes and in human melanoma cells, PPARb controls cellular proliferation and cell cycle progression and its depletion leads to cell cycle arrest. We also show that PPARb controls the response of normal human epidermal keratinocytes to UV-induced DNA damage. PPARb depletion decreases the expression and/or activation of multiple effectors of DNA Damage Response (DDR) pathway and favours the apoptotic response of human keratinocytes to UV irradiation. Our preclinical data of a PDX melanoma model demonstrated that the depletion or inhibition of PPARb delays of blocks tumor formation. Our data suggest that PPARb inhibition can be considered as a therapeutic target for the prevention of UV-induced skin cancers in vulnerable population, by attenuating the DDR and eliminating skin cells with high UV-induced mutational burden.
Published in
Transcriptional and functional regulation of cell cycle and UV response by PPARβ in human skin epidermal cells
Nguyen TN, Winkler C, Ginster S et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2024 · PMID 39620966 · doi:10.1096/fj.202401950R
This dataset
Open GSE263846 in finder → Find more human 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 GSE263846_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 PRJNA1099598 and SRA study SRP501417. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39620966) ↗
Study design
16 conditions, mostly in triplicate
Ctrl.NT.06h ×3 Ctrl.UV.06h ×3 PP2.NT.06h ×3 PP2.UV.06h ×3 PPB.NT.06h ×3 PPB.UV.06h ×3 PPD.NT.06h ×3 PPD.UV.06h ×3 +8 more

Supports a between-group comparison across 48 samples.

How we read this: 16 replicated groups read from 48 sample titles; they account for 48 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

+ 8 more — browse all 48 samples with per-sample file links →

Datasets on a similar topic

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