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. 2021 Aug 24;8:711227. doi: 10.3389/fmolb.2021.711227

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Copyright © 2021 Ruiz, Libedinsky and Elorza.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of copper action in cancer. (A) The high energy demand found in these cells decreases the oxygen concentrations, producing hypoxia; this causes an increase in the transmembrane transporter CTR1, which causes an increase of the intracellular concentrations of copper. The levels of this metal together with the reduced concentration of oxygen can stabilize and activate the HIF-1 transcription factor, triggering the activation of genes related to growth and tumor development. On the other hand, the high copper content promotes the assembly of complex IV (COX1) which is followed by the upregulation of OXPHOS. A higher oxygen demand will induce the upregulation of HIF1-alpha, creating a virtuous cycle for tumor growth. Excess of copper will also up regulate ATOX1 expression to promote cell proliferation as well. HRE: hypoxia-response Element. EMT: epithelial–mesenchymal Transition.