Skeletal muscle atrophy is attenuated in tumor-bearing mice under chemotherapy by treatment with fish oil and selenium

Oncotarget. 2015 Apr 10;6(10):7758-73. doi: 10.18632/oncotarget.3483.

Abstract

Chemotherapy can cause cachexia, which is manifested by weight loss, inflammation and muscle atrophy. However, the mechanisms of tumor and chemotherapy on skeletal muscle proteolysis, remained unclear. In this report, we demonstrated that tumor-induced myostatin in turn induced TNF-α, thus activating calcium-dependent and proteasomal protein degradation. Chemotherapy activated myostatin-mediated proteolysis and muscle atrophy by elevating IL-6. In tumor-bearing mice under chemotherapy, supplementation with fish oil and selenium prevented a rise in IL-6, TNF-α and myostatin and muscle atrophy. The findings presented here allow us to better understand the molecular basis of cancer cachexia and potentiate nutrition supplementation in future cancer chemotherapy.

Keywords: cachexia; chemotherapy; fish oil; muscle atrophy; selenium.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Atrophy
  • Cachexia / chemically induced*
  • Cachexia / metabolism*
  • Cachexia / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cricetinae
  • Docetaxel
  • Fish Oils / pharmacology*
  • Interleukin-6 / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Muscle, Skeletal / drug effects*
  • Muscle, Skeletal / pathology*
  • Myostatin / metabolism
  • Selenium / pharmacology*
  • Taxoids / adverse effects
  • Taxoids / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Fish Oils
  • Interleukin-6
  • Mstn protein, mouse
  • Myostatin
  • Taxoids
  • Tumor Necrosis Factor-alpha
  • Docetaxel
  • Selenium