bims-cytox1 Biomed news
on Cytochrome oxidase subunit 1
Issue of 2018‒09‒02
two papers selected by
Gavin McStay
Staffordshire University


  1. Adv Clin Chem. 2018 ;pii: S0065-2423(18)30032-5. [Epub ahead of print]86 127-155
    Ilie IR.
      Polycystic ovary syndrome (PCOS) is a common female endocrine disorder, which still remains largely unsolved in terms of etiology and pathogenesis despite important advances in our understanding of its genetic, epigenetic, or environmental factor implications. It is a heterogeneous disease, frequently associated with insulin resistance, chronic inflammation, and oxidative stress and probably accompanied with subclinical cardiovascular disease (CVD) and some malignant lesions as well, such as endometrial cancer. Discrepancies in the clinical phenotype and progression of PCOS exist between different population groups, which nuclear genetic studies have so far failed to explain. Over the last years, mitochondrial dysfunction has been increasingly recognized as an important contributor to an array of diseases. Because mitochondria are under the dual genetic control of both the mitochondrial and nuclear genomes, mutations within either DNA molecule may result in deficiency in respiratory chain function that leads to a reduced ability to produce cellular adenosine-5'-triphosphate and to an excessive production of reactive oxygen species. However, the association between variants in mitochondrial genome, mitochondrial dysfunction, and PCOS has been investigated to a lesser extent. May mutations in mitochondrial DNA (mtDNA) become an additional target of investigations on the missing PCOS heritability? Are mutations in mtDNA implicated in the initiation and progression of PCOS complications, e.g., CVDs, diabetes mellitus, cancers?
    Keywords:  Mitochondrial; Mitochondrial dysfunction; Oxidative stress; Polycystic ovary syndrome; mtDNA mutations
    DOI:  https://doi.org/10.1016/bs.acc.2018.05.003
  2. Transl Res. 2018 Jul 31. pii: S1931-5244(18)30114-2. [Epub ahead of print]
    Pustylnikov S, Costabile F, Beghi S, Faccibene A.
      An essential advantage during eukaryotic cell evolution was the acquisition of a network of mitochondria as a source of energy for cell metabolism and contrary to conventional wisdom, functional mitochondria are essential for the cancer cell. Multiple aspects of mitochondrial biology beyond bioenergetics support transformation including mitochondrial biogenesis, fission and fusion dynamics, cell death susceptibility, oxidative stress regulation, metabolism, and signaling. In cancer, the metabolism of cells is reprogrammed for energy generation from oxidative phosphorylation to aerobic glycolysis and impacts cancer mitochondrial function. Furthermore cancer cells can also modulate energy metabolism within the cancer microenvironment including immune cells and induce "metabolic anergy" of antitumor immune response. Classical approaches targeting the mitochondria of cancer cells usually aim at inducing changing energy metabolism or directly affecting functions of mitochondrial antiapoptotic proteins but most of such approaches miss the required specificity of action and carry important side effects. Several types of cancers harbor somatic mitochondrial DNA mutations and specific immune response to mutated mitochondrial proteins has been observed. An attractive alternative way to target the mitochondria in cancer cells is the induction of an adaptive immune response against mutated mitochondrial proteins. Here, we review the cancer cell-intrinsic and cell-extrinsic mechanisms through which mitochondria influence all steps of oncogenesis, with a focus on the therapeutic potential of targeting mitochondrial DNA mutations or Tumor Associated Mitochondria Antigens using the immune system.
    DOI:  https://doi.org/10.1016/j.trsl.2018.07.013