Cited by 134Muscle Physiology and DisordersNutrition and Health in AgingMuscle metabolism and nutrition

Protein breakdown in cancer cachexia

Sandri, Marco·2016·Seminars in Cell & Developmental Biology

Abstract

Skeletal muscle is a highly adaptive tissue, capable of altering muscle fiber size, functional capacity and metabolism in response to physiological stimuli. However, pathological conditions such as cancer growth compromise the mechanisms that regulate muscle homeostasis, resulting in loss of muscle mass, functional impairment and compromised metabolism. This tumor-induced condition is characterized by enhanced muscle protein breakdown and amino acids release that sustain liver gluconeogenesis and tissue protein synthesis. Proteolysis is controlled by the two most important cellular degradation systems, the ubiquitin proteasome and autophagy lysosome. These systems are carefully regulated by different signalling pathways that determine protein and organelle turnover. In this review we will describe the involvement of the ubiquitin proteasome and autophagy lysosome systems in cancer cachexia and the principal signalling pathways that regulate tumor-induced protein breakdown in muscle.

Integrity signals

Registry

Crossref · 10.1016/j.semcdb.2015.11.002

Cites

151 of 151 references verified0 citation errors · 0 not checkable

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  • Muscle loss in DKO mice is due to FoxO-mediated activation of the ubiquitin-proteasome system together with impairment of general autophagy and mitophagy pathways.

    “Mechanistically, muscle loss is due to FoxO-mediated activation of the ubiquitin–proteasome system together with the impairment of general autophagy and mitophagy pathways [25,31,32].”

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Authors
Sandri, M.
Affiliations
University of Padua (IT)
Corresponding author
Sandri, Marco
Venue
Seminars in Cell & Developmental Biology
Publisher
Elsevier BV
Published
2016-06
Volume
54
Pages
11-19
ISSN
1084-9521 (ISSN-L)
OpenAlex
W2118708400
Cited by
134
References
151
Citations by year
2026: 8 · 2025: 5 · 2024: 11 · 2023: 7 · 2022: 17 · 2021: 20 · 2020: 9 · 2019: 20 · 2018: 19 · 2017: 9 · 2016: 9
FWCI
1.20
Type
journal article
Language
en
Open access
closed
Locations
  • Seminars in Cell and Developmental Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Padua Research Archive (University of Padova) (submittedVersion)
Funders
  • Fondation Leducq
  • Ministero dell’Istruzione, dell’Università e della Ricerca
  • European Research Council (282310-MyoPHAGY)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
Keywords
cancer cachexia, skeletal muscle, muscle protein degradation, ubiquitin-proteasome system, autophagy, muscle homeostasis, amino acid release, liver gluconeogenesis, protein synthesis, signaling pathways, muscle atrophy
MeSH terms
Animals, Cachexia, Humans, Muscular Atrophy, Neoplasms, Proteins, Signal Transduction, Proteolysis

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