Colon 26 adenocarcinoma (C26)-induced cancer cachexia impairs skeletal muscle mitochondrial function and content

• Published in: Journal of muscle research and cell motility Vol. 40; no. 1; pp. 59 - 65
• Main Authors: Neyroud, Daria, Nosacka, Rachel L., Judge, Andrew R., Hepple, Russell T.
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.03.2019; Springer Nature B.V
• Subjects: Adenocarcinoma; Adenosine; Animal Anatomy; Biomedical and Life Sciences; Biomedicine; Body weight; Cachexia; Cancer; Cell Biology; Colon; Electron transport; Histology; Life Sciences; Mitochondria; Morphology; Musculoskeletal system; Proteomics; Rapid Communication; Respiration; Skeletal muscle; Mitochondrial respiration; Oxidative phosphorylation; Mitochondrial homeostasis; Muscle wasting; Mitochondrial content; Mitochondrial coupling
• ISSN: 0142-4319; 1573-2657
• DOI: 10.1007/s10974-019-09510-4

The present study aimed to determine the impact of colon 26 adenocarcinoma (C26)-induced cancer cachexia on skeletal muscle mitochondrial respiration and content. Twelve male CD2F1 mice were injected with C26-cells (tumor bearing (TB) group), whereas 12 age-matched mice received PBS vehicle injection (non-tumor bearing (N-TB) group). Mitochondrial respiration was studied in saponin-permeabilized soleus myofibers. TB mice showed lower body weight (~ 20%) as well as lower soleus , gastrocnemius - plantaris complex and tibialis anterior masses versus N-TB mice (p < 0.05). Soleus maximal state III mitochondrial respiration was 20% lower (10 mM glutamate, 5 mM malate, 5 mM adenosine diphosphate; p < 0.05) and acceptor control ratio (state III/state II) was 15% lower in the TB vs. N-TB (p < 0.05), with the latter suggesting uncoupling. Lower VDAC protein content suggested reduced mitochondrial content in TB versus N-TB (p < 0.05). Skeletal muscle in C26-induced cancer cachexia exhibits reductions in: maximal mitochondrial respiration capacity, mitochondrial coupling and mitochondrial content.