Cited by 563Nutrition and Health in AgingMuscle Physiology and DisordersAdipose Tissue and Metabolism

Understanding cachexia as a cancer metabolism syndrome

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Porporato, P E·2016·Oncogenesis

Abstract

Metabolic reprogramming occurs in tumors to foster cancer cell proliferation, survival and metastasis, but as well at a systemic level affecting the whole organism, eventually leading to cancer cachexia. Indeed, as cancer cells rely on external sources of nitrogen and carbon skeleton to grow, systemic metabolic deregulation promoting tissue wasting and metabolites mobilization ultimately supports tumor growth. Cachectic patients experience a wide range of symptoms affecting several organ functions such as muscle, liver, brain, immune system and heart, collectively decreasing patients’ quality of life and worsening their prognosis. Moreover, cachexia is estimated to be the direct cause of at least 20% of cancer deaths. The main aspect of cachexia syndrome is the unstoppable skeletal muscle and fat storage wasting, even with an adequate caloric intake, resulting in nutrient mobilization – both directly as lipid and amino acids and indirectly as glucose derived from the exploitation of liver gluconeogenesis – that reaches the tumor through the bloodstream. From a metabolic standpoint, cachectic host develops a wide range of dysfunctions, from increased insulin and IGF-1 resistance to induction of mitochondrial uncoupling proteins and fat tissue browning resulting in an increased energy expenditure and heat generation, even at rest. For a long time, cachexia has been merely considered an epiphenomenon of end-stage tumors. However, in specific tumor types, such as pancreatic cancers, it is now clear that patients present markers of tissue wasting at a stage in which tumor is not yet clinically detectable, and that host amino acid supply is required for tumor growth. Indeed, tumor cells actively promote tissue wasting by secreting specific factors such as parathyroid hormone-related protein and micro RNAs. Understanding the molecular and metabolic mediators of cachexia will not only advance therapeutic approaches against cancer, but also improve patients’ quality of life.

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Authors
Porporato, P. E.
Affiliations
UCLouvain (BE)
Corresponding author
Porporato, P E
Venue
Oncogenesis
Published
2016-02-22
Volume
5
Issue
2
Pages
e200-e200
ISSN
2157-9024 (ISSN-L)
OpenAlex
W2279428213
Cited by
562
References
202
Citations by year
2026: 40 · 2025: 45 · 2024: 53 · 2023: 57 · 2022: 55 · 2021: 68 · 2020: 81 · 2019: 62 · 2018: 56 · 2017: 32 · 2016: 13
FWCI
6.37
Type
journal article
Language
en
Open access
Locations
  • Oncogenesis (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Institutional Research Information System University of Turin (University of Turin) (submittedVersion, cc-by)
  • Digital Access to Libraries (submittedVersion, other-oa)
Funders
  • Fondation Louvain
  • Fonds De La Recherche Scientifique - FNRS
  • Belgian Federal Science Policy Office (Attraction Pole (IAP) grant #UP7-03, UP7-03)
  • Fédération Wallonie-Bruxelles (ARC 14/19–058, 14/19-058)
  • Servier
  • FP7 Ideas: European Research Council (243188)
Topics
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
cancer cachexia, cancer metabolism, metabolic reprogramming, skeletal muscle atrophy, nutrient mobilization, gluconeogenesis, insulin resistance, IGF-1 resistance, mitochondrial uncoupling, brown adipose tissue browning, pancreatic cancer, parathyroid hormone-related protein, microRNA

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