HSP72 functionally inhibits the anti-neoplastic effects of HDAC inhibitors

Histone deacetylase inhibitors (HDACi) enhance the acetylation of both histones and non-histone proteins, and induce apoptosis. They are potential therapeutic agents for the treatment of lymphoid neoplasms, but, with an overall remission rate of approximately 30%, they exhibit limited effectiveness [1–4]. The molecular mechanisms underlying the variability in HDACi sensitivity remain largely unknown; however, HR23B, a candidate biomarker for HDACi sensitivity [5], has been shown to regulate HDACi-induced apoptosis and autophagy [6].