Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling
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Maria Peiris-Pagès1,3, Gloria Bonuccelli2,3, Federica Sotgia2,3 and Michael P. Lisanti2,3
1Clinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK
2Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, UK
3The Paterson Institute, University of Manchester, Withington, UK
Federica Sotgia, email: firstname.lastname@example.org
Michael P. Lisanti, email: email@example.com
Keywords: mitochondrial fission; OXPHOS; cancer stem-like cells (CSCs); cell migration; metastasis
Received: December 12, 2017 Accepted: January 09, 2018 Published: January 19, 2018
Mitochondria are dynamic organelles frequently undergoing fission and fusion events to maintain their integrity, bioenergetics and spatial distribution, which is fundamental to the processes of cell survival. Disruption in mitochondrial dynamics plays a role in cancer. Therefore, proteins involved in regulating mitochondrial dynamics are potential targets for treatment. mDIVI1 is an inhibitor of the mitochondrial fission protein DRP1, which induces i) mitochondrial oxidative stress and ii) effectively reduces mitochondrial metabolism. We show here that mDIVI1 is able to inhibit 3D tumorsphere forming capacity, cell migration and stemness-related signalling in breast cancer cells, indicating that mDIVI1 can potentially be used for the therapeutic elimination of cancer stem cells (CSCs).
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