p53 connects tumorigenesis and reprogramming to pluripotency.
The tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of p53 was described to facilitate nuclear reprogramming. These findings suggest an influence of p53 on the de-differentiation process, and highlight the similarities between induction of pluripotency and tumor formation.
Tapia
Natalia
N
Department of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Münster 48149, Germany.
Schöler
Hans R
HR
D000818:Animals; D054337:Cell Dedifferentiation; D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D065150:Cellular Reprogramming / Q000235:genetics*; D006801:Humans; D057026:Induced Pluripotent Stem Cells / Q000473:pathology / Q000502:physiology*; D009369:Neoplasms / Q000235:genetics / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
D016159:Tumor Suppressor Protein p53