Cancer cell metastasis relies on processes that consume large amounts of ATP, such as actomyosin contractility and the rapid cycling of actin monomers during rearrangements of the cytoskeleton. This would suggest that metabolic strategies that best support the energetic demands of a migrating cell could be a contributing factor in the invasion and metastasis of cancer cells. We explored limiting ATP generation by manipulating mitochondria directly with loss-of-function and mitochondria isolation and transfer experiments.