From Pathogens to Cancer: Are Cancer Cells Evolved Mitochondrial Super Cells?

Abstract

Life is based on a highly specific combination of atoms, metabolism, and genetics which eventually reflects the chemistry of the Universe which is composed of hydrogen, oxygen, nitrogen, sulfur, phosphorus, and carbon. The interaction of atomic, metabolic, and genetic cycles results in the organization and de-organization of chemical information of that which we consider as living entities, including cancer cells. In order to approach the problem of the origin of cancer it is therefore reasonable to start from the assumption that the sub-molecular level, the atomic structure, should be the considered starting point on which metabolism, genetics, and external insults eventually emanate. Second, it is crucial to characterize which of the entities and parts composing human cells may live a separate life; certainly, this theoretical standpoint would consider mitochondria, an organelle of “bacteria” origin embedded in conditions favorable for the onset of both. This organelle has not only been tolerated by immunity but has also been placed as a central regulator of cell defense. Virus, bacteria, and mitochondria are also similar in the light of genetic and metabolic elements; they share not only equivalent DNA and RNA features but also many basic biological activities. Thus, it is important to finalize that once the cellular integrity has been constantly broken down, the mitochondria like any other virus or bacteria return to their original autonomy to simply survive. The Warburg’s law that states the ability of cancers to ferment glucose in the presence of oxygen, indicates mitochondria respiration abnormalities may be the underlying cause of this transformation towards super cancer cells. Though genetic events play a key part in altering biochemical metabolism, inducing aerobic glycolysis, this is not enough to impair mitochondrial function since mitochondrial biogenesis and quality control are constantly upregulated in cancers. While some cancers have mutations in the nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle, enzymes that produce oncogenic metabolites, there is also a bio-physic pathway for pathogenic mitochondrial genome mutations. The atomic level of all biological activities can be considered the very beginning, marked by the electron abnormal behavior that consequently affects DNA of both cells and mitochondria. Whilst the cell’s nucleus DNA after a certain number of errors and defection tends to gradually switch off, the mitochondria DNA starts adopting several escape strategies, switching-on a few important genes that belong back at their original roots as independent beings. The ability to adopt this survival trick, by becoming completely immune to current life-threatening events, is probably the beginning of a differentiation process towards a “super-power cell”, the cancer cells that remind many pathogens, including virus, bacteria, and fungi. Thus, here, we present a hypothesis regarding those changes that first begin at the mitochondria atomic level to steadily involve molecular, tissue and organ levels in response to the virus or bacteria constant insults that drive a mitochondria itself to become an “immortal cancer cell”. Improved insights into this interplay between these pathogens and mitochondria progression may disclose newly epistemological paradigms as well as innovative procedures in targeting cancer cell progressive invasion.

Mitochondrial Deoxyribonucleic Acid (mtDNA), Maternal Inheritance, and Their Role in the Development of Cancers: A Scoping Review

“…Studies have noted that mtDNA mutations, dysregulation of mtDNA, and disturbances in the communication between nuclear DNA and mtDNA may affect cellular health and in turn, predispose to carcinogenesis [ 54 ]. A recent hypothesis also suggested that the mitochondria may under the influence of microbial pathogens can transform themselves into super-power cells or immortal cancer cells that enable tumor formation [ 55 ]. In view of the potential role of mtDNA in aging and diseases including cancers, the role of gene editing in therapeutic management was being explored [ 56 ].…”

The effect of therapeutic communication based on Peplau’s model on body image and pain among cancer patients undergoing radiotherapy in the Parsian hospital of Shahrekord

“…In other words, cancer is clinically caused by the uncontrolled growth of several cells. It may metastasize to other parts of the body (4). There are various cancer treatments, depending on the cancer type and how advanced it is, such as surgery, radiation therapy, chemotherapy, targeted therapy, and precision medicine.…”

COVID-19 on Oral Health: A New Bilateral Connection for the Pandemic

“…Some in vitro evidence indicates that another entry factor that potentiates SARS-CoV-2 s infectivity [14] is represented by neuropilin-1 (NRP-1), a signaling protein highly present in the O.C. In addition to the well-known roles played by ACE2 and TMPRSS2, additional endosomal proteases (CTSB, CTSL, and BSG) and tissue-specific proteases (TMPRSS4 and TMPRSS11D) might facilitate the virus s entrance into cells for intracellular reproduction [15,16]. Interaction of the cell membrane-based receptor ACE2 of the host cell with the spike protein of SARS-CoV-2 triggers the endosomal pathway internalization, which results in virus endocytosis [13,17].…”