Hypoxia-induced immortalization of primary cells depends on Tfcp2L1 expression.

ABSTRACT: Cellular senescence is a stress response mechanism that induces proliferative arrest. Hypoxia can bypass senescence and extend the lifespan of primary cells, mainly by decreasing oxidative damage. However, how hypoxia promotes these effects prior to malignant transformation is unknown. Here we observed that the lifespan of mouse embryonic fibroblasts (MEFs) is increased when they are cultured in hypoxia by reducing the expression of p16^INK4a, p15^INK4b and p21^Cip1. We found that proliferating MEFs in hypoxia overexpress Tfcp2l1, which is a main regulator of pluripotency and self-renewal in embryonic stem cells, as well as stemness genes including Oct3/4, Sox2 and Nanog. Tfcp2l1 expression is lost during culture in normoxia, and its expression in hypoxia is r

SUBMITTER: Otero-Albiol D 

PROVIDER: S-EPMC10902313 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature