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Updated: Jun 16, 2025
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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
Published on: November 30, 2016
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Cancer-induced FOXP1 disrupts and reprograms skeletal-muscle circadian transcription in cachexia
Jeremy B Ducharme1, Daria Neyroud2, Martin M Schonk2
1Department of Physical Therapy, University of Florida, Gainesville, FL, USA; Myology Institute, University of Florida, Gainesville, FL, USA; University of Florida Health Cancer Center, Gainesville, FL, USA.
Cell Reports
|May 11, 2025
Summary
Cancer cachexia causes muscle wasting by disrupting the skeletal muscle clock. Forkhead box P1 (FoxP1) reprograms gene expression, impacting metabolism and contributing to this debilitating condition.
Area of Science:
- Molecular Biology
- Metabolic Disorders
- Cancer Research
Background:
- Cancer cachexia is a severe metabolic disorder causing significant muscle and body mass loss.
- Previous research identified Forkhead box P1 (FoxP1) upregulation in skeletal muscle as a driver of cancer-induced muscle wasting.
- The specific transcriptional networks regulated by FoxP1 in this context were not fully understood.
Purpose of the Study:
- To investigate the role of FoxP1 in regulating the skeletal muscle circadian clock during cancer cachexia.
- To identify the transcriptional networks targeted by FoxP1 in skeletal muscle experiencing cancer-induced wasting.
- To understand how FoxP1 disrupts circadian gene expression patterns in muscle at the onset of cachexia.
Main Methods:
- Analysis of transcriptional networks regulated by FoxP1 in skeletal muscle.
- Investigating the impact of cancer-induced FoxP1 on the skeletal muscle circadian transcriptome.
- Examining the reprogramming of metabolic pathways (glucose, lipid, oxidative) governed by the circadian clock.
Main Results:
- FoxP1 acts as a key disruptor of the skeletal muscle circadian clock in response to cancer.
- Cancer-induced FoxP1 rewires the skeletal muscle circadian transcriptome, promoting pathways linked to muscle wasting.
- Disruption of temporal patterns in glucose, lipid, and oxidative metabolism pathways was observed.
Conclusions:
- FoxP1 plays a critical role in reprogramming the skeletal muscle circadian transcriptome during cancer cachexia.
- These cancer/disease-specific functions of FoxP1 contribute to muscle wasting and the development of cachexia.
- Targeting FoxP1's role in circadian disruption may offer therapeutic strategies for cancer cachexia.
Keywords:
CP: CancerChIP-seqRNA-seqcancer cachexiacircadian rhythminflammationmetabolismmuscle atrophymuscle clockpancreatic cancerskeletal muscleMore Related Videos
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