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Non-cytotoxic copper overload boosts mitochondrial energy metabolism to modulate cell proliferation and differentiation in the human erythroleukemic cell line K562
dc.contributor.author | Ruiz L.M. | |
dc.contributor.author | Jensen E.L. | |
dc.contributor.author | Rossel Y. | |
dc.contributor.author | Puas G.I. | |
dc.contributor.author | Gonzalez-Ibanez A.M. | |
dc.contributor.author | Bustos R.I. | |
dc.contributor.author | Ferrick D.A. | |
dc.contributor.author | Elorza A.A. | |
dc.date.accessioned | 2020-09-02T22:27:32Z | |
dc.date.available | 2020-09-02T22:27:32Z | |
dc.date.issued | 2016 | |
dc.identifier | 10.1016/j.mito.2016.04.005 | |
dc.identifier.citation | 29, , 18-30 | |
dc.identifier.issn | 15677249 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/6112 | |
dc.description | Copper is integral to the mitochondrial respiratory complex IV and contributes to proliferation and differentiation, metabolic reprogramming and mitochondrial function. The K562 cell line was exposed to a non-cytotoxic copper overload to evaluate mitochondrial dynamics, function and cell fate. This induced higher rates of mitochondrial turnover given by an increase in mitochondrial fusion and fission events and in the autophagic flux. The appearance of smaller and condensed mitochondria was also observed. Bioenergetics activity included more respiratory complexes, higher oxygen consumption rate, superoxide production and ATP synthesis, with no decrease in membrane potential. Increased cell proliferation and inhibited differentiation also occurred. Non-cytotoxic copper levels can modify mitochondrial metabolism and cell fate, which could be used in cancer biology and regenerative medicine. © 2016 Elsevier B.V. and Mitochondria Research Society. | |
dc.language.iso | en | |
dc.publisher | Elsevier B.V. | |
dc.subject | Autophagy | |
dc.subject | Bioenergetics | |
dc.subject | Copper | |
dc.subject | Erythropoiesis | |
dc.subject | Mitochondria | |
dc.subject | Mitochondrial dynamics | |
dc.subject | adenosine triphosphate | |
dc.subject | copper | |
dc.subject | reactive oxygen metabolite | |
dc.subject | copper | |
dc.subject | aerobic metabolism | |
dc.subject | Article | |
dc.subject | autophagy | |
dc.subject | bioenergy | |
dc.subject | cell differentiation | |
dc.subject | cell fate | |
dc.subject | cell function | |
dc.subject | cell proliferation | |
dc.subject | cell structure | |
dc.subject | controlled study | |
dc.subject | copper overload | |
dc.subject | energy metabolism | |
dc.subject | enzyme synthesis | |
dc.subject | erythroleukemia cell | |
dc.subject | human | |
dc.subject | human cell | |
dc.subject | mitochondrial dynamics | |
dc.subject | mitochondrial membrane potential | |
dc.subject | mitochondrial respiration | |
dc.subject | nutritional disorder | |
dc.subject | oxygen consumption | |
dc.subject | priority journal | |
dc.subject | upregulation | |
dc.subject | drug effects | |
dc.subject | energy metabolism | |
dc.subject | K-562 cell line | |
dc.subject | metabolism | |
dc.subject | mitochondrion | |
dc.subject | Cell Differentiation | |
dc.subject | Cell Proliferation | |
dc.subject | Copper | |
dc.subject | Energy Metabolism | |
dc.subject | Humans | |
dc.subject | K562 Cells | |
dc.subject | Mitochondria | |
dc.title | Non-cytotoxic copper overload boosts mitochondrial energy metabolism to modulate cell proliferation and differentiation in the human erythroleukemic cell line K562 | |
dc.type | Article |