Mitochondrial division inhibitor (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism

Mitochondrial division inhibitor (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism

Blog Article

Abstract Increasing evidence supports the hypothesis that cancer progression is under mitochondrial control.Mitochondrial fission plays a pivotal role in the maintenance of cancer cell homeostasis.The inhibition of DRP1, the main Lower Clamp Cover regulator of mitochondrial fission, with the mitochondrial division inhibitor (mdivi-1) had been associated with cancer cell sensitivity to chemotherapeutics and decrease proliferation.

Here, using breast cancer cells we find that mdivi-1 induces the detachment of the cells, leading to a bulk of floating cells that conserved their viability.Despite a decrease in their proliferative and clonogenic capabilities, these floating cells maintain the capacity to re-adhere upon re-seeding and retain their migratory and invasive potential.Interestingly, the cell detachment induced by mdivi-1 is independent of DRP1 but relies on inhibition of mitochondrial complex I.

Furthermore, mdivi-1 induces cell detachment rely on glucose and the pentose phosphate pathway.Our data evidence a novel DRP1-independent effect of mdivi-1 in the attachment of cancer cells.The generation of floating viable cells Electric Water Pumps restricts the use of mdivi-1 as a therapeutic agent and demonstrates that mdivi-1 effect on cancer cells are more complex than anticipated.