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A more recent version of this article appeared on January 13, 2006
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M511064200v1
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Papers In Press, published online ahead of print November 1, 2005
J. Biol. Chem, 10.1074/jbc.M511064200
Submitted on October 11, 2005
Accepted on November 1, 2005

Induction of oxidative metabolism by mitochondrial frataxin inhibits cancer growth: Otto Warburg revisited

Tim J. Schulz, René Thierbach, Anja Voigt, Gunnar Drewes, Brun H. Mietzner, Pablo Steinberg, Andreas F. H. Pfeiffer, and Michael Ristow

Human Nutrition, Univ. Jena, Inst. of Nutrition, Jena D-07743

Corresponding Author: jbc{at}mristow.org

More than 80 years ago Otto Warburg suggested that cancer might be caused by a decrease in mitochondrial energy metabolism paralleled by an increase in glycolytic flux. In later years, it was shown that cancer cells exhibit multiple alterations in mitochondrial content, structure, function, and activity. We have stably overexpressed the Friedreich’s ataxia-associated protein frataxin in several colon cancer cell lines. These cells have increased oxidative metabolism, as shown by concurrent increases in aconitase activity, mitochondrial membrane potential, cellular respiration, and ATP content. Consistent with Warburg’s hypothesis, frataxin-overexpressing cells also have decreased growth rates and population doubling times, show inhibited colony formation capacity in soft-agar assays, and exhibit a reduced capacity of tumor formation when injected into nude mice. Furthermore, overexpression of frataxin leads to an increased phosphorylation of the tumor suppressor p38 MAP kinase, as well as decreased phosphorylation of ERK. Taken together, these results support the view that an increase in oxidative metabolism induced by mitochondrial frataxin may inhibit cancer growth in mammals.


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