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      Mitochondria and Cancer

      research-article
      1 , 2 , 2 , 3 , 2 , 4
      Molecular cell

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          Abstract

          Decades ago Otto Warburg observed that cancers ferment glucose in the presence of oxygen, suggesting that defects in mitochondrial respiration may be the underlying cause of cancer. We now know that the genetic events, which drive aberrant cancer cell proliferation, also alter biochemical metabolism including promoting aerobic glycolysis, but do not typically impair mitochondrial function. Mitochondria supply energy, provide building blocks for new cells, and control redox homeostasis, oncogenic signaling, innate immunity and apoptosis. Indeed, mitochondrial biogenesis and quality control are often upregulated in cancers. While some cancers have mutations in nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle enzymes that produce oncogenic metabolites, there is negative selection for pathogenic mitochondrial genome mutations. Eliminating mitochondrial DNA limits tumorigenesis and rare human tumors with mutant mitochondrial genomes are relatively benign. Thus, mitochondria play a central and multi-functional role in malignant tumor progression, and targeting mitochondria provides therapeutic opportunities.

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          Author and article information

          Journal
          9802571
          20730
          Mol Cell
          Mol. Cell
          Molecular cell
          1097-2765
          1097-4164
          24 February 2016
          3 March 2016
          03 March 2017
          : 61
          : 5
          : 667-676
          Affiliations
          [1 ]Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, 164 Frelinghuysen Road, Piscataway, NJ 08854
          [2 ]Rutgers Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903
          [3 ]Lewis-Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Princeton, NJ 08544
          [4 ]Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ, 08854
          Author notes
          Corresponding Author: Dr. Eileen White, Rutgers Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903-2681, V: 732-235-5329, epwhite@ 123456cinj.rutgers.edu
          Article
          PMC4779192 PMC4779192 4779192 nihpa760143
          10.1016/j.molcel.2016.02.011
          4779192
          26942671
          27d16670-7cda-4424-a361-2882b315d6e3
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