Weisheng Xu

TL;DR: This review focuses on the mechanisms of action of histone deacetylase ( HDAC) inhibitors (HDACi), a group of recently discovered ‘targeted’ anticancer agents that induces different phenotypes in various transformed cells.

TL;DR: Effects of SAHA on p21(WAF1)-associated proteins are identified that explain, at least in part, the selective effect of HDACi in altering gene expression.

TL;DR: It is reported here that TBP-2 expression is reduced in human primary breast and colon tumors compared with adjacent tissue, and this results support a model in which the expression of a subset of genes is repressed in transformed cells, leading to a block in differentiation, and culture of transformed cells with SAHA causes re-expression of these genes, leads to induction of growth arrest, differentiate, and/or apoptosis.

TL;DR: It is found that the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a benzamide, cause an accumulation of reactive oxygen species (ROS) and caspase activation in transformed but not normal cells.

TL;DR: In this article, the redox regulatory proteins, peroxiredoxin (Prx) I and Prx II are specific targets of histone deacetylases (HDACs) and they are elevated in many cancers and neurodegenerative diseases.