Histone deacetylase inhibitor trichostatin a potentiates doxorubicin‐induced apoptosis by up‐regulating PTEN expression

Abstract

TSA promoted doxorubicin-induced apoptosis through a mechanism that involved the stimulation of Egr-1 expression, acetylation of core histones at the PTEN promoter, and consequently induction of PTEN transcription. These findings provide a theoretical basis for the therapeutic application of combined treatment of TSA/doxorubicin for cancer.