title: Disabling mitochondrial reprogramming in cancer.
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.
authors.affiliation: Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, United States.
authors.forename: M Cecilia
authors.initials: MC
authors.lastname: Caino
authors.affiliation: Prostate Cancer Discovery and Development Program, Tumor Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, United States. Electronic address: daltieri@wistar.org.
authors.forename: Dario C
authors.initials: DC
authors.lastname: Altieri
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002448:Cell Adhesion / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D022001:Focal Adhesions / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D019869:Phosphatidylinositol 3-Kinases
keywords: Drug resistance; Hsp90; Metastasis; Mitochondria; PI3K