Journal
EMBO REPORTS
Volume 18, Issue 2, Pages 334-343Publisher
WILEY
DOI: 10.15252/embr.201541922
Keywords
HDAC2; pancreatic ductal adenocarcinoma; primary cilia
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Funding
- JSPS [26112712, 15K07931, 15H01215]
- Kurata Memorial Hitachi Science and Technology Foundation
- Takeda Science Foundation
- Daiichi Sankyo Foundation of Life Science
- Sagawa Foundation for Promotion of Cancer Research
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Foundation for Nara Institute of Science and Technology
- NIH [R01HD069647, 9R01GM120776-05A1]
- Grants-in-Aid for Scientific Research [26112712, 15H01215, 15K07931] Funding Source: KAKEN
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Loss of primary cilia is frequently observed in tumor cells, including pancreatic ductal adenocarcinoma (PDAC) cells, suggesting that the absence of this organelle may promote tumorigenesis through aberrant signal transduction and the inability to exit the cell cycle. However, the molecular mechanisms that explain how PDAC cells lose primary cilia are still ambiguous. In this study, we found that inhibition or silencing of histone deacetylase 2 (HDAC2) restores primary cilia formation in PDAC cells. Inactivation of HDAC2 results in decreased Aurora A expression, which promotes disassembly of primary cilia. We further showed that HDAC2 controls ciliogenesis independently of Kras, which facilitates Aurora A expression. These studies suggest that HDAC2 is a novel regulator of primary cilium formation in PDAC cells.
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