Restoration of mitochondria function as a target for cancer therapy

Drug Discov Today. 2015 May;20(5):635-43. doi: 10.1016/j.drudis.2015.03.001. Epub 2015 Mar 9.

Abstract

Defective oxidative phosphorylation has a crucial role in the attenuation of mitochondrial function, which confers therapy resistance in cancer. Various factors, including endogenous heat shock proteins (HSPs) and exogenous agents such as dichloroacetate, restore respiratory and other physiological functions of mitochondria in cancer cells. Functional mitochondria might ultimately lead to the restoration of apoptosis in cancer cells that are refractory to current anticancer agents. Here, we summarize the key reasons contributing to mitochondria dysfunction in cancer cells and how restoration of mitochondrial function could be exploited for cancer therapeutics.

Publication types

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

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / therapeutic use*
  • Dichloroacetic Acid / chemistry
  • Dichloroacetic Acid / therapeutic use*
  • Drug Design
  • Energy Metabolism / drug effects*
  • Humans
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Molecular Targeted Therapy
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Oxidative Phosphorylation / drug effects
  • Signal Transduction / drug effects

Substances

  • Antineoplastic Agents
  • Dichloroacetic Acid