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Publication : DAXX silencing suppresses mouse ovarian surface epithelial cell growth by inducing senescence and DNA damage.

First Author  Pan WW Year  2013
Journal  Gene Volume  526
Issue  2 Pages  287-94
PubMed ID  23542781 Mgi Jnum  J:200730
Mgi Id  MGI:5509131 Doi  10.1016/j.gene.2013.03.103
Citation  Pan WW, et al. (2013) DAXX silencing suppresses mouse ovarian surface epithelial cell growth by inducing senescence and DNA damage. Gene 526(2):287-94
abstractText  Mouse ovarian surface epithelium (OSE) is a single layer of cubodial epithelial cells that covers the ovary surface and is involved in regulating the secretion and transport of 17beta-hydroxysteroid dehydrogenase. Recently, OSE cells have attracted particular interest as a major source of ovarian cancer. Death-associated protein DAXX along with PML (promyelocytic leukemia protein) nuclear bodies (PML-NBs) reportedly play roles in transcriptional regulation and apoptosis. However, little is known regarding a role for DAXX in mOSE cells. In this study, we both over-expressed DAXX and depleted DAXX in primary mOSE cells. We found that Daxx deletion accelerated senescence in a p53/p21-dependent manner and promoted DNA damage by interacting with PML bodies without affecting cell cycle progression. These results suggest that DAXX may transform mOSE cells to an ovarian oncogenic phenotype and may be an anti-cancer target.
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