Isfahan University of Medical Sciences Journal of Isfahan Medical School 1027-7595 32 283 2014 05 22 Mitochondria in Cancer Mitochondria in Cancer 590 597 14326 FA Massoud Houshmand Assistant Professor, Department of Medical Genetics, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran Elaheh Mosaieby Department of Medical Genetics, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran Journal Article 2013 12 10 The hypothesis that changes in oxidative phosphorylation induce by mitochondrial dysfunction involved in tumorgenesis is so long discussed. Mitochondrion is vital for cell proliferation and has irreversible central role in the apoptosis (programmed cell death). Furthermore, mtDNA mutations have been founded in various cancer cells; although, the role of mitochondrial DNA mutations remains largely unknown. The mitochondria mutations do not lead to its deactivation but these mutations can change biosynthesis, bioenergetics, signal transduction, transcription and chromatin structure of the cell. In this paper, the major impairment in mtDNA and its effect on tumorgenesis were discussed. The hypothesis that changes in oxidative phosphorylation induce by mitochondrial dysfunction involved in tumorgenesis is so long discussed. Mitochondrion is vital for cell proliferation and has irreversible central role in the apoptosis (programmed cell death). Furthermore, mtDNA mutations have been founded in various cancer cells; although, the role of mitochondrial DNA mutations remains largely unknown. The mitochondria mutations do not lead to its deactivation but these mutations can change biosynthesis, bioenergetics, signal transduction, transcription and chromatin structure of the cell. In this paper, the major impairment in mtDNA and its effect on tumorgenesis were discussed. https://jims.mui.ac.ir/article_14326_18d3284f148b6cb726b412b7059223ff.pdf