1α,25-dihydroxyvitamin D3 mitigates cancer cell mediated mitochondrial dysfunction in human skeletal muscle cells

Zachary C. Ryan, Theodore A. Craig, Xuewei Wang, Philippe Delmotte, Jeffrey L Salisbury, Ian R Lanza, Gary C Sieck, Rajiv Kumar

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Cancer cachexia is associated with muscle weakness and atrophy. We investigated whether 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3), which has previously been shown to increase skeletal myoblast oxygen consumption rate, could reverse the deleterious effects of tumor cell conditioned medium on myoblast function. Conditioned medium from Lewis lung carcinoma (LLC1) cells inhibits oxygen consumption, increases mitochondrial fragmentation, inhibits pyruvate dehydrogenase activity, and enhances proteasomal activity in human skeletal muscle myoblasts. 1α,25(OH)2D3 reverses the tumor cell-mediated changes in mitochondrial oxygen consumption and proteasomal activity, without changing pyruvate dehydrogenase activity. 1α,25(OH)2D3 might be useful in treatment of weakness seen in association with CC.

Original languageEnglish (US)
Pages (from-to)746-752
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume496
Issue number2
DOIs
StatePublished - Feb 5 2018

Keywords

  • 1α,25-dihydroxyvitamin D
  • Cancer
  • Gene expression
  • Mitochondria
  • Oxygen consumption
  • Skeletal muscle

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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