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Editorial
. 2014;13(3):347-8.
doi: 10.4161/cc.27513. Epub 2013 Dec 13.

Mitochondrial metabolism in TCA cycle mutant cancer cells

Lucas B Sullivan  1 , Navdeep S Chandel  1
Affiliations
Editorial

Mitochondrial metabolism in TCA cycle mutant cancer cells

Lucas B Sullivan et al. Cell Cycle. 2014.
No abstract available

Keywords: FH; GSF; HLRCC; ROS; TCA; fumarate; mitochondria cancer; reductive carboxylation.

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Figures

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Figure 1. FH mutant cancer cells maintain proliferation requirements supplied by the mitochondria. Normal cells utilize oxidative metabolism to supply metabolites for biosynthesis, ATP for energy, and ROS for signaling. FH-null cells supply these intermediates despite having impaired mitochondrial function. Biosynthetic citrate is produced by reductive carboxylation, ATP levels are maintained by glycolysis, and ROS levels are increased by fumarate accumulation.
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References

    1. Wallace DC. Nat Rev Cancer. 2012;12:685–98. doi: 10.1038/nrc3365. - DOI - PMC - PubMed
    1. Yang Y, et al. Cancer Genet Cytogenet. 2010;196:45–55. doi: 10.1016/j.cancergencyto.2009.08.018. - DOI - PMC - PubMed
    1. Mullen AR, et al. Nature. 2012;481:385–8. - PMC - PubMed
    1. Sena LA, et al. Mol Cell. 2012;48:158–67. doi: 10.1016/j.molcel.2012.09.025. - DOI - PMC - PubMed
    1. Sullivan LB, et al. Mol Cell. 2013;51:236–48. doi: 10.1016/j.molcel.2013.05.003. - DOI - PMC - PubMed

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