Histone deacetylase 6: at the interface of cancer and neurodegeneration

With the recognition in the early 1960s that histones can be post-translationally modified, the list of different post-translational modifications of histones and their biological consequences has continued to expand. In addition, the idea of the 'histone code' hypothesis, later introduced by David Allis and colleagues, further broaden the horizon of chromatin biology. Currently, there is a wealth of knowledge about the transition between the active and the repressive state of chromatin, and modifications of histones remains at the center of chromatin biology. Histone deacetylases (HDACs) in particular are of great importance for the therapeutic success of cancer treatment. Focusing primarily on HDAC6, herein we have briefly highlighted its unique involvement in cancer and also apparently in neurodegeneration. Cancer (uncontrolled cell proliferation) and neurodegenerative diseases (loss of neurons/protein aggregation) are two distinct pathological conditions that share/overlap certain molecular determinants. Histone deacetylase 6 appears to be one such determinant for which researchers have made significant progress by accumulating sufficient evidence for its clinical translation in these aforementioned disease conditions. Be it cancer or neurodegeneration, understanding the dynamics of histone modifications continues to be of great interest, and histone deacetylase 6 (HDAC6) now apparently is at the forefront.

Automated summary

With increasing knowledge about histone modifications and its role in disease conditions like cancer and neurodegeneration, histone deacetylase 6 (HDAC6) is considered to be at the forefront of research advancing clinical translation in these areas.