ArticleCell reports2025
Cancer-induced FOXP1 disrupts and reprograms skeletal-muscle circadian transcription in cachexia.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Stable clocks, rewired rhythms: circadian remodeling in skeletal muscle during aging, cachexia, and type 2 diabetes.Life metabolism · 2026Review
- Pancreatic Cancer Disrupts Circadian Patterns of Gene Expression in Cardiorespiratory Muscles.Journal of cachexia, sarcopenia and muscle · 2026Article
- Co-expression network analysis reveals repression ofbioRxiv : the preprint server for biology · 2026Article
- Cancer therapy and cachexia.The Journal of clinical investigation · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
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 toward 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.