Poster

Mitochondrial function and cancer

May 2012

Mitochondria undertake multiple critical functions in a cell. In addition to compartmentalizing the metabolic pathways and physiological states of the cell, the mitochondria generate much of the cellular energy, regulate the cellular redox state, produce most of the cellular reactive oxygen species (ROS), buffer cellular Ca2+ and initiate cellular apoptosis. Mitochondria were first proposed to be relevant to cancer by Otto Warburg who reported that cancer cells exhibited "aerobic-glycolysis". Although this was originally interpreted as indicating that the function of mitochondria was defective, we now understand that cancer cells are in an altered metabolic state. Little attention has been paid to the potential mutations that can affect mitochondrial function in cancer, outside of specific mutations in genes such as fumarate hydratase (FH), which is associated with a rare cancer syndrome, hereditary leiomyomatosis and renal cell carcinoma (HLRCC). Genes such as FH are encoded in the nuclear DNA, so once mutated they affect all mitochondria in a cell. However, mitochondria also have their own DNA and mutations in mitochondrial genes are common and have been shown to be involved in human diseases, such as mitochondrial myopathy. The resurgence of interest in metabolism in cancer cells has started to focus attention back on the mitochondria and there is increasing evidence that mutations in mitochondrial DNA encoded genes can contribute to the development of cancer. It is possible that such mutations provide metabolic adaptivity to the cancer cell. This poster, covers our current understanding of the contribution of mitochondrial function to cancer cell metabolism. The editorial content of this poster was conceived and developed by the poster author Douglas C. Wallace, and the editorial team at Nature Reviews Cancer.

This poster is freely available thanks to support from Abcam.

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