Non-cytotoxic copper overload boosts mitochondrial energy metabolism to modulate cell proliferation and differentiation in the human erythroleukemic cell line K562

Lina M. Ruiz, Erik L. Jensen, Yancing Rossel, German I. Puas, Alvaro M. Gonzalez-Ibanez, Rodrigo I. Bustos, David A. Ferrick, Alvaro A. Elorza

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)18-30
Number of pages13
JournalMitochondrion
Volume29
DOIs
Publication statusPublished - 1 Jul 2016

Keywords

  • Autophagy
  • Bioenergetics
  • Copper
  • Erythropoiesis
  • Mitochondria
  • Mitochondrial dynamics

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology

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