SIRT1-NOX4 signaling axis regulates cancer cachexia

J Exp Med. 2020 Jul 6;217(7):e20190745. doi: 10.1084/jem.20190745.

Abstract

Approximately one third of cancer patients die due to complexities related to cachexia. However, the mechanisms of cachexia and the potential therapeutic interventions remain poorly studied. We observed a significant positive correlation between SIRT1 expression and muscle fiber cross-sectional area in pancreatic cancer patients. Rescuing Sirt1 expression by exogenous expression or pharmacological agents reverted cancer cell-induced myotube wasting in culture conditions and mouse models. RNA-seq and follow-up analyses showed cancer cell-mediated SIRT1 loss induced NF-κB signaling in cachectic muscles that enhanced the expression of FOXO transcription factors and NADPH oxidase 4 (Nox4), a key regulator of reactive oxygen species production. Additionally, we observed a negative correlation between NOX4 expression and skeletal muscle fiber cross-sectional area in pancreatic cancer patients. Knocking out Nox4 in skeletal muscles or pharmacological blockade of Nox4 activity abrogated tumor-induced cachexia in mice. Thus, we conclude that targeting the Sirt1-Nox4 axis in muscles is an effective therapeutic intervention for mitigating pancreatic cancer-induced cachexia.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / pathology
  • Animals
  • Cachexia / complications*
  • Cachexia / metabolism*
  • Cell Line
  • Cell Line, Tumor
  • Disease Models, Animal
  • Disease Progression
  • Forkhead Transcription Factors / metabolism
  • HEK293 Cells
  • Humans
  • Metabolome / drug effects
  • Mice
  • Muscle Fibers, Skeletal / drug effects
  • Muscle Fibers, Skeletal / metabolism
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology
  • Muscular Atrophy / metabolism
  • Muscular Atrophy / pathology
  • NADPH Oxidase 4 / metabolism*
  • NF-kappa B / metabolism
  • Neoplasms / complications*
  • Neoplasms / metabolism*
  • Oxidation-Reduction
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Protein Stability / drug effects
  • Reactive Oxygen Species / metabolism
  • Resveratrol / pharmacology
  • Signal Transduction* / drug effects
  • Sirtuin 1 / metabolism*
  • Wasting Syndrome / pathology

Substances

  • Forkhead Transcription Factors
  • NF-kappa B
  • Reactive Oxygen Species
  • NADPH Oxidase 4
  • Sirtuin 1
  • Resveratrol