Abstract
In the first part of our study, we substantiated that the embryonic reontogenesis and malignant growth (disintegrating growth) pathways are the same, but occur at different stages of ontogenesis, this mechanism is carried out in opposite directions. Cancer has been shown to be epigenetic-blocked redifferentiation and unfinished somatic embryogenesis. We formulated that only this approach of aging elimination has real prospects for a future that is fraught with cancer, as we will be able to convert this risk into a rejuvenation process through the continuous cycling of cell dedifferentiation–differentiation processes (permanent remorphogenesis). Here, we continue to develop the idea of looped ontogenesis and formulate the concept of the rejuvenation circle.
Highlights
Full-scale reprogramming that never turns into cancer does not have a full-fledged biological alternative for simultaneously solving two main problems: eliminating both cancer and aging
Definitions IG – integrating growth, defined here as the submission of potency of single cells composing an organism to the development program and functions of the whole organism
All the authors reviewed, revised and approved the final version of the manuscript
Summary
Any methods affecting both individual ‘aging’ mechanisms and age-related pathology will only alleviate the burden of aging, and these diseases slow down their progression but will eliminate neither aging nor age-related diseases. At a later stage, the accumulation of 133p53α protects cells from death due to its antiapoptotic function and provides genetic stability, contributing to the restoration of DNA double stand breaks [89] It has been reported [90,91] that 133p53α plays an important role in embryogenesis and ESC, through sequentially expressing significant levels of 133p53α (at least ten-times higher than human fibroblasts). NKX3-1 replaces exogenous OCT4 to reprogram both mouse and human fibroblasts with comparable efficiency and to generate completely pluripotent stem cells [98] Another so-called oncogene and Yamanaka factor, c-Myc, when overexpressed could lead to opposite effects, for example, the inhibition of proliferative pathways [99] with the restoration of p53 function. As a result of this blocking, instead of the circle of rejuvenation, we switch to the ‘death gear’ of cancer (Figure 2B)
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