Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling | Zendy

Maria PeirisPagès | Zendy; Gloria Bonuccelli | Zendy; Federica Sotgia | Zendy; Michael P. Lisanti | Zendy

Open Access

Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling

Author(s) -

Maria PeirisPagès,

Gloria Bonuccelli,

Federica Sotgia,

Michael P. Lisanti

Publication year - 2018

Publication title -

oncotarget

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.373

H-Index - 127

ISSN - 1949-2553

DOI - 10.18632/oncotarget.24285

Subject(s) - mitochondrial fission , mitochondrial fusion , microbiology and biotechnology , mitochondrion , cancer stem cell , stem cell , cancer cell , biology , cell , cancer research , bioenergetics , cancer , chemistry , mitochondrial dna , biochemistry , genetics , gene

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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