1,493
Views
23
CrossRef citations to date
0
Altmetric
Research Paper

Mitochondria-targeted antioxidant SkQ1 suppresses fibrosarcoma and rhabdomyosarcoma tumour cell growth

, ORCID Icon, , , , , , ORCID Icon, , & ORCID Icon show all
Pages 1797-1811 | Received 04 Jun 2018, Accepted 22 Jun 2018, Published online: 31 Jul 2018

References

  • Chandel NS. Mitochondria as signaling organelles. BMC Biol. 2014;12:34.
  • Fruehauf JP, Meyskens FL. Reactive oxygen species: a breath of life or death? Clin. Cancer Res. 2007;13:789–794.
  • Guzman-Villanueva D, Weissig V. Mitochondria-Targeted Agents: mitochondriotropics, Mitochondriotoxics, and Mitocans. Handb Exp Pharmacol. 2017;240:423–438.
  • Modica-Napolitano JS, Aprille JR. Delocalized lipophilic cations selectively target the mitochondria of carcinoma cells. Adv Drug Deliv Rev. 2001;49:63–70.
  • Sabharwal S, Schumacker P. Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel? Nat Rev Cancer. 2014;14:709–721.
  • Agapova LS, Chernyak BV, Domnina LV, et al. Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 3. Inhibitory effect of SkQ1 on tumor development from p53-deficient cells. Biochemistry (Mosc). 2008;73:1300–1316.
  • Shagieva G, Domnina L, Makarevich O, et al. Depletion of mitochondrial reactive oxygen species downregulates epithelial-to-mesenchymal transition in cervical cancer cells. Oncotarget. 2017;8:4901–4913.
  • Skulachev VP, Anisimov VN, Antonenko YN, et al. An attempt to prevent senescence: A mitochondrial approach. Biochim Biophys Acta Bioenerg. 2009;1787:437–461.
  • Severina II, Severin FF, Korshunova GA, et al. In search of novel highly active mitochondria-targeted antioxidants: thymoquinone and its cationic derivatives. FEBS Lett. 2013;587:2018–2024.
  • Rao VA, Klein SR, Bonar SJ, et al. The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinone. J Biol Chem. 2010;285:34447–34459.
  • Starenki D, Park J-I. Mitochondria-targeted nitroxide, Mito-CP, suppresses medullary thyroid carcinoma cell survival in vitro and in vivo. J Clin Endocrinol Metab. 2013;98:1529–1540.
  • Cheng G, Zielonka J, McAllister DM, et al. Mitochondria-targeted vitamin E analogs inhibit breast cancer cell energy metabolism and promote cell death. BMC Cancer. 2013;13:285.
  • Vandekerckhove J, Weber K. At least six different actins are expressed in a higher mammal: an analysis based on the amino acid sequence of the amino-terminal tryptic peptide. J Mol Biol. 1978;126:783–802.
  • Dugina V, Zwaenepoel I, Gabbiani G, et al. Beta and gamma-cytoplasmic actins display distinct distribution and functional diversity. J Cell Sci. 2009;122:2980–2988.
  • Dugina V, Khromova N, Rybko V, et al. Tumor promotion by γ and suppression by β non-muscle actin isoforms. Oncotarget. 2015;6:14556–14571.
  • Antonenko Y, Avetisyan A, Bakeeva L, et al. Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 1. Cationic plastoquinone derivatives: synthesis and in vitro studies. Biochem (Mosc). 2008;73:1273–1287.
  • Popova EN, Pletjushkina OY, Dugina VB, et al. Scavenging of Reactive Oxygen Species in Mitochondria Induces Myofibroblast Differentiation. Antioxid Redox Signal. 2010;13:1297–1307.
  • Littlepage LE, Ruderman JV. Identification of a new APC/C recognition domain, the A box, which is required for the Cdh1-dependent destruction of the kinase Aurora-A during mitotic exit. Genes Dev. 2002;16:2274–2285.
  • Stewart S, Fang G. Destruction box-dependent degradation of aurora B is mediated by the anaphase-promoting complex/cyclosome and Cdh1. Cancer Res. 2005;65:8730–8735.
  • Kumari G, Ulrich T, Krause M, et al. Induction of p21CIP1 protein and cell cycle arrest after inhibition of Aurora B kinase is attributed to aneuploidy and reactive oxygen species. J Biol Chem. 2014;289:16072–16084.
  • Shagieva GS, Domnina LV, Chipysheva TA, et al. Actin isoforms and reorganization of adhesion junctions in epithelial-to-mesenchymal transition of cervical carcinoma cells. Biochem (Mosc). 2012;77:1266–1276.
  • Shinohara M, Shang W-H, Kubodera M, et al. Nox1 redox signaling mediates oncogenic Ras-induced disruption of stress fibers and focal adhesions by down-regulating Rho. J Biol Chem. 2007;282:17640–17648.
  • Alexandrova AY, Dugina VB, Paterson H, et al. Motility of intracellular particles in rat fibroblasts is greatly enhanced by phorbol ester and by over-expression of normal p21N-ras. Cell Motil Cytoskeleton. 1993;25:254–266.
  • Paterson H, Reeves B, Brown R, et al. Activated N-ras controls the transformed phenotype of HT1080 human fibrosarcoma cells. Cell. 1987;51:803–812.
  • Archer H, Bar-Sagi D. Ras and Rac as Activators of Reactive Oxygen Species (ROS). GTPase Protoc New Jersey: Humana Press. 2002;189:067–073.
  • Serù R, Mondola P, Damiano S, et al. HaRas activates the NADPH oxidase complex in human neuroblastoma cells via extracellular signal-regulated kinase 1/2 pathway. J Neurochem. 2004;91:613–622.
  • Alexandrova AY, Kopnin PB, Vasiliev JM, et al. ROS up-regulation mediates Ras-induced changes of cell morphology and motility. Exp Cell Res. 2006;312:2066–2073.
  • Baldini E, Sorrenti S, Da E, et al. Aurora kinases: new molecular targets in thyroid cancer therapy. Clin Ter. 2012;163:e457–62.
  • Anand S, Penrhyn-Lowe S, Venkitaraman AR. AURORA-A amplification overrides the mitotic spindle assembly checkpoint, inducing resistance to Taxol. Cancer Cell. 2003;3:51–62.
  • Carmena M, Earnshaw WC. The cellular geography of Aurora kinases. Nat Rev Mol Cell Biol. 2003;4:842–854.
  • Marumoto T, Honda S, Hara T, et al. Aurora-A kinase maintains the fidelity of early and late mitotic events in HeLa cells. J Biol Chem. 2003;278:51786–51795.
  • Yokoyama T, Goto H, Izawa I, et al. Aurora-B and Rho-kinase/ROCK, the two cleavage furrow kinases, independently regulate the progression of cytokinesis: possible existence of a novel cleavage furrow kinase phosphorylates ezrin/radixin/moesin (ERM). Genes Cells. 2005;10:127–137.
  • Hauf S, Cole RW, LaTerra S, et al. The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint. J Cell Biol. 2003;161:281–294.
  • Gully CP, Zhang F, Chen J, et al. Antineoplastic effects of an Aurora B kinase inhibitor in breast cancer. Mol Cancer. 2010;9:42.
  • Fernandez-Miranda G, Trakala M, Martin J, et al. Genetic disruption of aurora B uncovers an essential role for aurora C during early mammalian development. Development. 2011;138:2661–2672.
  • Han EH, Min J-Y, Yoo S-A, et al. A small-molecule inhibitor targeting the AURKC-IκBα interaction decreases transformed growth of MDA-MB-231 breast cancer cells. Oncotarget. 2017;8:69691–69708.
  • Sherr CJ. Cancer cell cycles. Science. 1996;274:1672–1677.
  • Topham CH, Taylor SS. Mitosis and apoptosis: how is the balance set? Curr Opin Cell Biol. 2013;25:780–785.
  • Vitale I, Galluzzi L, Castedo M, et al. Mitotic catastrophe: a mechanism for avoiding genomic instability. Nat Rev Mol Cell Biol. 2011;12:385–392.
  • Gupta S, Stanbridge EJ. Paired human fibrosarcoma cell lines that possess or lack endogenous mutant N-ras alleles as experimental model for Ras signaling pathways. Methods Enzymol. 2001;333:290–306.
  • McAllister RM, Melnyk J, Finklestein JZ, et al. Cultivation in vitro of cells derived from a human rhabdomyosarcoma. Cancer. 1969;24:520–526.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.