DAXX silencing suppresses mouse ovarian surface epithelial cell growth by inducing senescence and DNA damage.
作者： Wei-Wei Pan , Fa-Ping Yi , Li-Xian Cao , Xiao-Man Liu , Zhong-Fei Shen
DOI: 10.1016/J.GENE.2013.03.103
关键词:
摘要: Mouse ovarian surface epithelium (OSE) is a single layer of cubodial epithelial cells that covers the ovary and involved in regulating secretion transport 17β-hydroxysteroid dehydrogenase. Recently, OSE have attracted particular interest as major source cancer. Death-associated protein DAXX along with PML (promyelocytic leukemia protein) nuclear bodies (PML-NBs) reportedly play roles transcriptional regulation apoptosis. However, little known regarding role for mOSE cells. In this study, we both over-expressed depleted primary We found Daxx deletion accelerated senescence p53/p21-dependent manner promoted DNA damage by interacting without affecting cell cycle progression. These results suggest may transform to an oncogenic phenotype be anti-cancer target.
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