Research Article Integrative Molecular Medicine Volume 6: 1-3 Integr Mol Med, 2019 doi: 10.15761/IMM.1000356 ISSN: 2056-6360 Te role of mitochondria in tumorigenesis Mouza Mohammed AlFashti AlAleeli* Department of Medical Diagnostics, Sheikh Khalifa Medical City - Ajman, Ministry of Presidential Affairs, United Arab Emirates Abstract Te maternal inheritance of the mitochondrial DNA is one of its amazing characteristics. It is located in the matrix of a mitochondrion. Te cellular organelle that is responsible for the generation of ATPs is the mitochondrion. A lot of studies have linked the mitochondria with the generation of cancer cells. Tere is a crosstalk in the medical research feld that whether the cancer cells were originated from a nuclear defect or from a mitochondrial dysfunction. In this review paper, I will highlight the role of mitochondria in tumorigenesis. Introduction Te mitochondrial genome, which is the DNA of the mitochondria, is strictly inherited maternally, it is a 16569 base pair long circular double stranded DNA (heavy strand from the outside and light strand from the inside), which has a coding region and non-coding region [it is called the control region that consists of Hypervariable Region 1 (HV1) and Hypervariable Region 2 (HV2)], and the coding region codes for 2 ribosomal RNA genes, 22 transfer RNA genes, and 13 protein- coding sequences [2 subunits of ATP synthase, 3 cytochrome oxidase subunits, 7 NADH dehydrogenase subunits and one cytochrome b] that are involved in the electron transport chain [1]. Te mitochondria are the organelles of the cytoplasm, they have double membranes [an outer membrane and inner membrane, and in between an inter- membrane space], the ATP synthase and the electron transport chain proteins are located on the inner membrane of the mitochondria [2]. Te mitochondria are responsible for the energy production that fuels the entire cells, which is represented by the generation of adenosine triphosphates [ATPs], those are formed by oxidative phosphorylation process, which is known as the citric acid cycle in the mitochondria [1]. Moreover, there are other mitochondrial proteins that are not directed by the mitochondrial genome, the nuclear DNA might encode for proteins to be synthesized in the ribosomes of the mitochondria [2]. In this review paper, I will discuss the role of mitochondria in tumorigenesis by linking the origin and the mechanism of the tumor cells with the function of the mitochondria in leading to those fundamental concepts. Cancer as a mitochondrial metabolic disease Dogma roles! Cancer is a genetic disease. Te dogma is irrefutable truth, it is a concept that it is no longer challenged or investigated; the dogma is solid. Hanahan & Weinberg have solidifed this dogma when they have published a paper titled as “Hallmarks of Cancer: Te Next Generation” on 2011. As they have declared, the somatic mutation theory is the foundation of the dogma, which means that cancer cells proliferate in an accelerated rate due to mutations in genes [tumor suppressor genes or proto-oncogenes] that inhibit or stimulate cell division, and they have preserved the dogma when they have claimed that cancer cells have dysregulated energy metabolism that are controlled by proliferation-inducing oncogenes [3]. Tis means that cancer cell is purely result from a defect in the nuclear DNA of a *Correspondence to: Mouza Mohammed AlFashti AlAleeli, Medical Laboratory Scientist, Department of Medical Diagnostics, Sheikh Khalifa Medical City - Ajman, Ministry of Presidential Afairs, United Arab Emirates, Tel: 00971507347878; E-mail: TeMuse1992@hotmail.com Received: January 15, 2019; Accepted: February 04, 2019; Published: February 06, 2019 normal cell. Another example of maintaining the dogma is the work of Stratton, Campbell, & Futreal, which have already mentioned in their published paper “Te cancer genome.” on 2009 that cancer cells are raised from series of chance mutations, and they have predict that the minimum accumulation of 4 random mutations in a normal cell will be enough to transform it to a cancer cell [4]. Seyfried, Flores, Pof, & D’Agostino have questioned the dogma, when they have published a paper on 2014 “Cancer as a metabolic disease: implications for novel therapeutics”, they have emphasized that metastasis of the cancer occurs in a stepwise cascade, the cancer cells 1) invade to the local tissues, 2) enter into the circulation, 3) survive the immune system, 4) immunosuppress the immune system, 5) leave the circulation, 6) form secondary tumors, and this is a non- random metastatic cascade, which is hard to imagine that it is caused by random somatic mutations [14]. Tey have collected the previous experimental studies that have challenged the somatic mutation theory; in order to draw their conclusion. One of their selections is the work of McKinnell, Deggins, & Labat, they have transplanted the nucleus of a renal tumor cell from a triploid frog into enucleated eggs, those eggs have matured to become a tadpole, but cannot further diferentiate to triploid frog, and the tadpole [which was cloned from the nucleus of a frog renal cell tumor] was clear from any tumor [6]. Another work that have been highlighted is the research of Li, Connelly, Wetmore, Curran, & Morgan, they have studied medulloblastoma [which is a brain tumor] by transplanting its nuclei into embryonic stem cells, the results were that those embryonic stem cells stopped diferentiation and there was no sign of medulloblastoma [7]. Hochedlinger, et al. published a paper “Reprogramming of a melanoma genome by nuclear transplantation” on 2004, they took the melanoma tumors and characterized genetically the mutations that were in the melanoma genome, then they transplanted the nuclei of the melanoma tumors into embryonic stem cells; to clone the mice,