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

doi:10.1016/j.bbrc.2018.01.092

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 journal › Article › peer-review

8 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 language	English (US)
Pages (from-to)	746-752
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	496
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2018.01.092
State	Published - 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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10.1016/j.bbrc.2018.01.092

Cite this

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

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.",

keywords = "1α,25-dihydroxyvitamin D, Cancer, Gene expression, Mitochondria, Oxygen consumption, Skeletal muscle",

author = "Ryan, {Zachary C.} and Craig, {Theodore A.} and Xuewei Wang and Philippe Delmotte and Salisbury, {Jeffrey L.} and Lanza, {Ian R.} and Sieck, {Gary C.} and Rajiv Kumar",

note = "Publisher Copyright: {\textcopyright} 2018 The Author(s)",

year = "2018",

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doi = "10.1016/j.bbrc.2018.01.092",

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T1 - 1α,25-dihydroxyvitamin D3 mitigates cancer cell mediated mitochondrial dysfunction in human skeletal muscle cells

AU - Ryan, Zachary C.

AU - Craig, Theodore A.

AU - Wang, Xuewei

AU - Delmotte, Philippe

AU - Salisbury, Jeffrey L.

AU - Lanza, Ian R.

AU - Sieck, Gary C.

AU - Kumar, Rajiv

PY - 2018/2/5

Y1 - 2018/2/5

N2 - 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.

AB - 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.

KW - 1α,25-dihydroxyvitamin D

KW - Cancer

KW - Gene expression

KW - Mitochondria

KW - Oxygen consumption

KW - Skeletal muscle

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