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Int. J. Mol. Sci. 2013, 14(5), 9514-9535; doi:10.3390/ijms14059514

HDAC6 and Ovarian Cancer

Department of Pathology and Cell Biology, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA
Program of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Dr., Tampa, FL 33612, USA
Author to whom correspondence should be addressed.
Received: 2 April 2013 / Revised: 23 April 2013 / Accepted: 24 April 2013 / Published: 2 May 2013
(This article belongs to the Special Issue Genes and Pathways in the Pathogenesis of Ovarian Cancer)
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The special class IIb histone deacetylase, HDAC6, plays a prominent role in many cellular processes related to cancer, including oncogenesis, the cell stress response, motility, and myriad signaling pathways. Many of the lessons learned from other cancers can be applied to ovarian cancer as well. HDAC6 interacts with diverse proteins such as HSP90, cortactin, tubulin, dynein, p300, Bax, and GRK2 in both the nucleus and cytoplasm to carry out these cancerous functions. Not all pro-cancer interactions of HDAC6 involve deacetylation. The idea of using HDAC6 as a target for cancer treatment continues to expand in recent years, and more potent and specific HDAC6 inhibitors are required to effectively down-regulate the tumor-prone cell signaling pathways responsible for ovarian cancer.
Keywords: HDAC6; ovarian cancer; cancer-related signaling pathways; HDAC6 inhibitors; cell stress response; motility; oncogenesis; histone deacetylase HDAC6; ovarian cancer; cancer-related signaling pathways; HDAC6 inhibitors; cell stress response; motility; oncogenesis; histone deacetylase
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Haakenson, J.; Zhang, X. HDAC6 and Ovarian Cancer. Int. J. Mol. Sci. 2013, 14, 9514-9535.

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