P53-guided response to nucleostemin loss in normal versus cancer cells.

R Y L Tsai

doi:10.1038/cddis.2015.377

Abstract

p53-guided response to nucleostemin loss in normal versus cancer cells.

Highlights

Stem cells play pivotal roles in organogenesis, tissue regeneration, aging, and cancer formation
Earlier studies have indicated that mammalian NS contributes to p53 inactivation via physical interaction with MDM2.8,9 Yet the need of p53 for NS to perform its obligatory function is disputed by multiple groups, who show that NS remains indispensable for p53-null cancer cells[2] and that NS loss triggers DNA damage to the same extent in p53-wild type as in p53-null mouse embryonic fibroblast (MEF) cells.[5]
In MEF cells, NS depletion leads to G2 arrest regardless of their p53 status, but causes a marked increase of polyploid giant cells (PGCs) only in the absence of p53

Summary

Introduction

Stem cells play pivotal roles in organogenesis, tissue regeneration, aging, and cancer formation. Earlier studies have indicated that mammalian NS contributes to p53 inactivation via physical interaction with MDM2.8,9 Yet the need of p53 for NS to perform its obligatory function is disputed by multiple groups, who show that NS remains indispensable for p53-null cancer cells[2] and that NS loss triggers DNA damage to the same extent in p53-wild type as in p53-null mouse embryonic fibroblast (MEF) cells.[5] Despite that, those who decide to adopt this view would still need to explain why some outcomes of NS-deficient cells appear to be shaped in a p53-dependent manner.

Results

Conclusion