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

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.
AuthorsWei-Wei Pan, Fa-Ping Yi, Li-Xian Cao, Xiao-Man Liu, Zhong-Fei Shen, You-Quan Bu, Ying Xu, Heng-Yu Fan, Fang-Zhou Song
JournalGene (Gene) Vol. 526 Issue 2 Pg. 287-94 (Sep 10 2013) ISSN: 1879-0038 [Electronic] Netherlands
PMID23542781 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Elsevier B.V. All rights reserved.
Chemical References
  • Carrier Proteins
  • Co-Repressor Proteins
  • Daxx protein, mouse
  • Intracellular Signaling Peptides and Proteins
  • Molecular Chaperones
  • Nuclear Proteins
  • Promyelocytic Leukemia Protein
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • PML protein, human
  • Oncogene Protein p21(ras)
Topics
  • Animals
  • Carcinoma, Ovarian Epithelial
  • Carrier Proteins (genetics, metabolism)
  • Cell Cycle (genetics)
  • Cellular Senescence (genetics)
  • Co-Repressor Proteins
  • DNA Damage
  • Epithelial Cells (metabolism)
  • Female
  • Gene Deletion
  • Gene Expression
  • Gene Silencing
  • Humans
  • Intracellular Signaling Peptides and Proteins (genetics, metabolism)
  • Mice
  • Molecular Chaperones
  • Neoplasms, Glandular and Epithelial (genetics, metabolism)
  • Nuclear Proteins (genetics, metabolism)
  • Oncogene Protein p21(ras) (genetics, metabolism)
  • Ovarian Neoplasms (genetics, metabolism)
  • Ovary (cytology, metabolism)
  • Promyelocytic Leukemia Protein
  • Transcription Factors (metabolism)
  • Tumor Suppressor Protein p53 (genetics, metabolism)
  • Tumor Suppressor Proteins (metabolism)

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