1α,25-dihydroxyvitamin D3 mitigates cancer cell mediated mitochondrial dysfunction in human skeletal muscle cells
Year: 2018
Type: article
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.
Institution: Mayo Clinic
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,110
Awards: Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosis, Live Unrelated Kidney Donor &Sibling Follow-up Study, Role of Mitochondria in Airway Smooth Muscle, Assessing Long Term Outcomes of Living Donation, Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosis, G9000223804
OpenAlex ID: W2788131567