The Role of HDAC6 in Cancer

Abstract

Histone deacetylase 6 (HDAC6), a member of the HDAC family whose major substrate is α ‐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.

Cited by papers we hold 6

• Insights into the post-translational modification and its emerging role in shaping the tumor microenvironment · 2021
  Corrected
• Impact of HDAC Inhibitors on Protein Quality Control Systems: Consequences for Precision Medicine in Malignant Disease · 2020
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• Selective HDAC6 inhibitors improve anti-PD-1 immune checkpoint blockade therapy by decreasing the anti-inflammatory phenotype of macrophages and down-regulation of immunosuppressive proteins in tumor cells · 2019
  Corrected
• Histone deacetylase 6 in cancer · 2018
  No notice
• Resveratrol as a Pan-HDAC Inhibitor Alters the Acetylation Status of Jistone Proteins in Human-Derived Hepatoblastoma Cells · 2013
  Corrected
• Roles of histone deacetylases in epigenetic regulation: emerging paradigms from studies with inhibitors · 2012
  No notice

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