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dc.contributor.authorPeiris-Pagès, Maria
dc.contributor.authorBonuccelli, Gloria
dc.contributor.authorSotgia, Federica
dc.contributor.authorLisanti, Michael P
dc.date.accessioned2018-05-05T21:34:40Z
dc.date.available2018-05-05T21:34:40Z
dc.date.issued2018-03-02
dc.identifier.citationMitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling. 2018, 9(17): 13254-13275 Oncotargeten
dc.identifier.issn1949-2553
dc.identifier.pmid29568355
dc.identifier.doi10.18632/oncotarget.24285
dc.identifier.urihttp://hdl.handle.net/10541/620988
dc.description.abstractMitochondria 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).
dc.language.isoenen
dc.rightsArchived with thanks to Oncotargeten
dc.titleMitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling.en
dc.typeArticleen
dc.contributor.departmentClinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UKen
dc.identifier.journalOncotargeten
refterms.dateFOA2018-12-17T15:21:43Z
html.description.abstractMitochondria 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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