Background:

Trichostatin A (TSA) is a potent inhibitor of histone deacetylase (HDAC) as well as an antifungal antibiotic with cytostatic and differentiating properties that noncompetivively and reversibly inhibits HDAC, at low nanomolar concentrations, in both cultured mammalian cells and fractionated cell nuclear extracts. It is capable of arresting cells in G₁and G₂phases of the cell cycle, inducing differentiation and reverting the transformed morphology of cells in culture. According to a study investigating the effect of TSA in human breast cancer cell lines, TSA inhibited proliferation of breast carcinoma cell lines (IC₅₀124.4 ± 120.4 nM), comparing to all cell lines (IC₅₀2.4 ± 0.5 nM), and resulted in pronounced histone H4 hyperacetylation.

Reference

[1].David M. Vigushin, Simak Ali, Paul E. Pace, Nina Mirsaidi, Kazuhiro Ito, Ian Adcock, and R. Charles Coombes. Trichostatin A is a histone deacetylase inhibitor with potent antitumot activity against breast cancer in vivo. Clin Cancer Res 2001;7:971-976