Mitochondrial substrates in cancer: drivers or passengers?

Björn Kruspig; Boris Zhivotovsky; Vladimir Gogvadze

doi:10.1016/j.mito.2014.08.007

Mitochondrial substrates in cancer: drivers or passengers?

Mitochondrion. 2014 Nov:19 Pt A:8-19. doi: 10.1016/j.mito.2014.08.007. Epub 2014 Aug 30.

Authors

Björn Kruspig¹, Boris Zhivotovsky², Vladimir Gogvadze³

Affiliations

¹ Division of Toxicology, Institute of Environmental Medicine Karolinska Institutet, Box 210 171 77 Stockholm, Sweden.
² Division of Toxicology, Institute of Environmental Medicine Karolinska Institutet, Box 210 171 77 Stockholm, Sweden; MV Lomonosov Moscow State University, 119991 Moscow, Russia.
³ Division of Toxicology, Institute of Environmental Medicine Karolinska Institutet, Box 210 171 77 Stockholm, Sweden; MV Lomonosov Moscow State University, 119991 Moscow, Russia. Electronic address: Vladimir.Gogvadze@ki.se.

PMID: 25179741
DOI: 10.1016/j.mito.2014.08.007

Abstract

The majority of cancers demonstrate various tumor-specific metabolic aberrations, such as increased glycolysis even under aerobic conditions (Warburg effect), whereas mitochondrial metabolic activity and their contribution to cellular energy production are restrained. One of the most important mechanisms for this metabolic switch is the alteration in the abundance, utilization, and localization of various mitochondrial substrates. Numerous lines of evidence connect disturbances in mitochondrial metabolic pathways with tumorigenesis and provide an intriguing rationale for utilizing mitochondria as targets for anti-cancer therapy.

Keywords: Cancer; Cell death; Metabolism; Mitochondria; Therapy; Warburg Effect.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Antineoplastic Agents / pharmacology*
Energy Metabolism / physiology*
Humans
Mitochondria / drug effects
Mitochondria / metabolism*
Neoplasms / drug therapy*
Neoplasms / metabolism*

Substances

Antineoplastic Agents