Journal
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY
Volume -, Issue -, Pages -Publisher
HINDAWI PUBLISHING CORPORATION
DOI: 10.1155/2011/875824
Keywords
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Funding
- Leukemia and Lymphoma Society of America
- National Institutes of Health (NIH) [HL75826, HL83077]
- William Lawrence and Blanche Hughes Foundation
- St. Baldrick's Foundation
- Eugene Cota-Robles Fellowship (ECR)
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075826, R01HL083077] Funding Source: NIH RePORTER
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Histone deacetylase 6 (HDAC6), a member of the HDAC family whose major substrate is a-tubulin, has become a target for drug development to treat cancer due to its major contribution in oncogenic cell transformation. Overexpression of HDAC6 correlates with tumorigenesis and improved survival; therefore, HDAC6 may be used as a marker for prognosis. Previous work demonstrated that in multiple myeloma cells, inhibition of HDAC6 results in apoptosis. Furthermore, HDAC6 is required for the activation of heat-shock factor 1 (HSF1), an activator of heat-shock protein encoding genes (HSPs) and CYLD, a cylindromatosis tumor suppressor gene. HDAC6 contributes to cancer metastasis since its upregulation increases cell motility in breast cancer MCF-7 cells and its interaction with cortactin regulates motility. HDAC6 also affects transcription and translation by regulating the heat-shock protein 90 (Hsp90) and stress granules (SGs), respectively. This review will discuss the role of HDAC6 in the pathogenesis and treatment of cancer.
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