International E-publication: Publish Projects, Dissertation, Theses, Books, Souvenir, Conference Proceeding with ISBN.  International E-Bulletin: Information/News regarding: Academics and Research

Mitochondrial Abnormalities and Pathways of Cancer

Author Affiliations

  • 1Department of Zoology, Nizam College, Hyderabad, AP, INDIA

Res. J. Recent Sci., Volume 3, Issue (ISC-2013), Pages 1-6, (2014)


Mitochondrial DNA (mtDNA) depletes mainly through damaged induced by DNA replication/reading errors and reactive oxygen species (ROS). Endothelial dysfunction (ED) is a result of increased oxidative stress, resulting from electron leakage in the biochemical reactions that occur in mitochondria, and leading to inhibition of nitric oxide (NO) production from endothelial nitric oxide synthase (eNOS). Dysfunction of eNOS leads to development of multiple forms of cancers. An increased reactive oxygen species (ROS) production causes mtDNA damage contributing to ED and accelerated ageing. This review explores an insight into mechanisms of mitochondrial dysfunction in cancer.


  1. Hanahan D. and Weinberg R.A., Hallmarks of cancer, The next generation, Cell., 144(5), 646-674 (2011)
  2. Shapovalov Y., Hoffman D., Zuch D., deMesy Bentley K.L. and Eliseev R.A., Mitochondrial dysfunction in cancer cells due to aberrant mitochondrial replication, J. Biol. Chem., 286, 22331-22338 (2011)
  3. Liang B.C., Evidence for association of mitochondrial DNA sequence amplification and nuclear localization in human low-grade gliomas, Mutat. Res., 354(1), 27-33 (1996)
  4. Brandes R. P., Fleming I. and Busse R., Endothelial aging, Cardiovasc. Res., 66(2), 286-294 (2005)
  5. Erusalimsky J. D., Vascular endothelial senescence: From mechanisms to pathophysiology, J. Appl. Physiol., 106(1), 326-332 (2009)
  6. Davidson S. M. and Duchen M. R., Endothelial mitochondria: Contributing to vascular function and disease, Circ. Res., 100(8), 1128-1141 (2007)
  7. Richard S.M., Bailliet G., Paez G.L., Bianchi M.S., Peltomaki P. and Bianchi N.O., Nuclear and mitochondrial genome instability in human breast cancer, Cancer Res., 60(15), 4231-4237 (2000)
  8. Gutierrez J., Ballinger S.W., Darley-Usmar V.M. and Landar A., Free radicals, mitochondria, and oxidized lipids, The emerging role in signal transduction in vascular cells, Circ. Res., 99(9), 924-932 (2006)
  9. Wei Y.H., Lu C.Y., Lee H.C., Pang C.Y., Ma Y.S., Oxidative damage and mutation to mitochondrial DNA and age-dependent decline of mitochondrial respiratory function, Ann. N.Y. Acad. Sci., 854, 155-170 (1998), 1-6 (2014)
  10. Duchen M.R., Mitochondria in health and diseases: perspectives on a new mitochondrial biology, Mol. Aspects. Med.,25(4), 365-45 (2004)
  11. Madamanchi N.R. and Runge M.S., Mitochondrial dysfunction in atherosclerosis, Circ. Res., 100(4), 460-473 (2007)
  12. Polyak K., Li Y., Zhu H., et al., Somatic mutations of the mitochondrial genome in human colorectal tumours, Nat. Genet., 20(3), 291-293 (1998)
  13. Burgart L.J., Zheng J., Shu Q., Strickler J.G. and Shibata D., Somatic mitochondrial mutation in gastric cancer, Am. J. Pathol., 147(4), 1105-1111 (1995)
  14. Wei Y.H., Oxidative stress and mitochondrial DNA mutations in human aging. Proc. Soc. Exp. Biol. Med.,217(1), 53-63 (1998)
  15. Modica-Napolitano J.S., Kulawiec M., and Singh K.K., Mitochondria and human Cancer, Curr Mole Med.,7, 121-131 (2007)
  16. Yamamoto H., Tanaka M., Katayama M., Obayashi T., Nimura Y. and Ozawa T., Significant existence of deleted mitochondrial DNA in cirrhotic liver surrounding hepatic tumor, Biochem. Biophys. Res. Commun., 182(2), 913-920 (1992)
  17. Clayton D.A. and Vinograd J., Complex mitochondrial DNA in leukemic and normal human myeloid cells, Proc. Natl. Acad. Sci. U. S. A., 62(4), 1077-1084 (1969)
  18. El Meziane A., Lehtinen S.K., Holt I. J. and Jacobs H.T., Mitochondrial tRNALeu isoforms in lung carcinoma cybrid cells containing the np 3243 mtDNA mutation, Hum. Mol. Genet., 7(13), 2141-2147 (1998)
  19. Heddi A., Faure-Vigny H., Wallace D.C. and Stepien G., Coordinate expression of nuclear and mitochondrial genes involved in energy production in carcinoma and oncocytoma, Biochim. Biophys. Acta., 1316(3), 203-209 (1996)
  20. Moncada S., Palmer R.M. and Higgs E.A., Nitric oxide: physiology, pathophysiology, and pharmacology, Pharmacol. Rev.,43, 109-142 (1991)
  21. Alderton W.K., Cooper C.E. and Knowles, R.G.,Nitric oxide synthases: structure, function and inhibitionBiochem. J, 357, 593-615 (2001)
  22. Cleeter M.W., Cooper J.M., Darley-Usmar V.M., Moncada S. and Schapira A.H.,Reversible inhibition of cytochrome c oxidase, the terminal enzyme of the mitochondrial respiratory chain, by nitric oxide, Implications for neurodegenerative diseases, FEBS, Lett., 34550-54 (1994)
  23. Clementi E., Brown G.C., Feelisch M. and Moncada. S., Persistent inhibition of cell respiration by nitric oxide: crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione. Proc. Natl. Acad. Sci. USA., 957631-763 (1998)
  24. Giulivi C., Poderoso J. J. and Boveris A., Production of nitric oxide by mitochondria, J. Biol. Chem., 273, 11038-11043 (1998)
  25. Goglia F., Moreno M. and Lanni A.,Action of thyroid hormones at the cellular level: the mitochondrial target,FEBS Lett., 452, 115-120(1999)
  26. Sangam S, Rajagopal S. and Joginapally V.R., Effect of mtDNA Depletion and Repletion on eNOS Expression in Human Endothelial Cells, Proceedings in Akademy of AndhraPradesh Sciences., Abstract 157 (2013)
  27. Chunxin W. and Youle R.J., The Role of Mitochondria in Apoptosis. Annu. Rev. Genetics., 43, 95-118 ( 2009)
  28. Panka D.J., Cho D.C., Atkins M.B. and Mier J.W., GSK-3beta inhibition enhances sorafenib-induced apoptosis in melanoma cell lines, J. Biol. Chem,.283, 726732 (2008)