AI Article Synopsis
- Mouse ovarian surface epithelium (OSE) consists of cuboidal epithelial cells that regulate hormone enzyme secretion and transport, and is linked to ovarian cancer.
- Recent research explores the role of the death-associated protein DAXX and PML nuclear bodies (PML-NBs) in OSE cells, particularly their impact on transcription and cell death.
- Findings indicate that removing DAXX speeds up cellular aging and DNA damage in mouse OSE cells, suggesting it could be a potential target for cancer treatment.
Article Abstract
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 17β-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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| http://dx.doi.org/10.1016/j.gene.2013.03.103 | DOI Listing |
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