Self-Protection of Cells from Damage: Is This Atavistic Mechanism Activated During the Development of Various Forms of Cancer?
摘要
This review analyzes the hypothesis of the retained abilities of various specialized mammalian cells to protect themselves from lethal damage by reactivating the protective atavistic mechanism of cellular plasticity. The development of such protection is accompanied by the transition of differentiated cells from an oxygen-dependent to an oxygen-independent type of metabolism. This transition increases the threshold of cell resistance to death under cancer-inducing damaging effects. At the same time, the level of cell differentiation decreases and embryonic markers appear. Such immature cells are necessary for the regeneration of damaged tissues. However, the regeneration programs of the embryo and the adult body differ significantly. As a result, the process of cellular redifferentiation would be forced to develop not in embryonic conditions but in “nonhealing wound” conditions, in which increases the risk of cancer initiation.