Disabling mitochondrial reprogramming in cancer

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Abstract

Recent studies have demonstrated that tumor cells exposed to molecular therapy with PI3K antagonists redistribute their mitochondria to the peripheral cytoskeleton, fueling membrane dynamics, turnover of focal adhesion complexes and increased tumor cell motility and invasion. Although this process paradoxically increases metastatic propensity during molecular therapy, it also emphasizes a critical role of regional mitochondrial bioenergetics in tumor metabolic reprogramming and may offer prime therapeutic opportunities to prevent disseminated disease.

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