Disabling mitochondrial reprogramming in cancer

Pharmacol Res. 2015 Dec:102:42-5. doi: 10.1016/j.phrs.2015.08.022. Epub 2015 Sep 10.

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.

Keywords: Drug resistance; Hsp90; Metastasis; Mitochondria; PI3K.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Cell Adhesion / drug effects
  • Cell Movement / drug effects
  • Cytoskeleton / drug effects
  • Cytoskeleton / metabolism
  • Cytoskeleton / pathology
  • Focal Adhesions / drug effects
  • Focal Adhesions / metabolism
  • Focal Adhesions / pathology
  • Humans
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Phosphatidylinositol 3-Kinases / metabolism

Substances

  • Antineoplastic Agents
  • Phosphatidylinositol 3-Kinases