Senescent cells and cancer cells as apoptosis suppressors: Causes and effects

Abstract

The death of some senescent cells (KS), as well as neoplastic cells (KN), can be paradoxically inhibited at the stage of apoptosis. Thus, the KS become inhibitors of oncogenesis at the beginning of the phenomenon. The influence of KS and KN on the inhibition of apoptosis is multidirectional, which is presented graphically in the form of Euler’s mathematical circles (Fig. 2). Senescence, like apoptosis, may to some extent inhibit oncogenesis. The neoplastic process is also associated with non-apoptotic death, i.e. entosis, as well as autophagy, i.e. autophagocytosis with the participation of lysosomes. The process of autophagy may also involve the cell proteolytic system via the ubiquitin-proteasome system (UPS), in which polyubiquitination of suppressor proteins, e.g. p53 protein, leads to oncogenesis. Therefore, both of the above-mentioned processes of autophagy favour oncogenesis. The paper also presents the role of human endogenous retroviruses (HERs) in oncogenesis, with particular emphasis on the syncytin gene and its participation in the induction of placental cancer (choriocarcinoma, chorioepithelioma).