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HDAC 2 promotes loss of primary cilia in pancreatic ductal adenocarcinoma
Author(s) -
Kobayashi Tetsuo,
Nakazono Kosuke,
Tokuda Mio,
Mashima Yu,
Dynlacht Brian David,
Itoh Hiroshi
Publication year - 2017
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201541922
Subject(s) - biological sciences , library science , chinese academy of sciences , history , biology , archaeology , china , computer science , computational biology
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 ( HDAC 2) restores primary cilia formation in PDAC cells. Inactivation of HDAC 2 results in decreased Aurora A expression, which promotes disassembly of primary cilia. We further showed that HDAC 2 controls ciliogenesis independently of Kras, which facilitates Aurora A expression. These studies suggest that HDAC 2 is a novel regulator of primary cilium formation in PDAC cells.