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Cancer-induced FOXP1 disrupts and reprograms skeletal muscle circadian transcription in cachexia [ChIP-seq]

GSE273712 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 7 samples Submitted 2025/05/11 Platform GPL19057
Summary
Cancer cachexia is a debilitating metabolic disorder characterized by involuntary loss of body and muscle mass, leading to increased morbidity and mortality. We previously found that Forkhead box P1 (FoxP1) upregulation in skeletal muscle causes muscle wasting and is required for muscle wasting in response to cancer. However, transcriptional networks targeted by FoxP1 in skeletal muscles undergoing cancer-induced wasting remain largely unknown. Here, we identify FoxP1 as a key disruptor of the skeletal muscle clock in response to cancer, that reprograms circadian patterns of gene expression at cachexia onset. Specifically, we show that cancer-induced FoxP1 rewires the skeletal muscle circadian transcriptome towards pathways associated with muscle wasting and disrupts the temporal patterning of pathways governing glucose, lipid, and oxidative metabolism. These findings thus implicate cancer/disease-specific functions of FOXP1 in the disruption and reprograming of the skeletal muscle circadian transcriptome which may contribute to muscle wasting and the development of cachexia.
Published in
Cancer-induced FOXP1 disrupts and reprograms skeletal-muscle circadian transcription in cachexia
Ducharme JB, Neyroud D, Schonk MM et al. · Cell reports 2025 · PMID 40349340 · doi:10.1016/j.celrep.2025.115689
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Direct links to NCBI, no account and no request form: the whole study as GSE273712_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 7 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1142901 and SRA study SRP523580. Searching any of these in the dataset finder brings you back here.

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