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Trichostatin A inhibits the proliferation of eight breast carcinoma cell lines including MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3 with mean IC50 of 124.4 nM (range, 26.4-308.1 nM), with more potency against cell lines that express ERα than the ERα-negative cell lines. Trichostatin A inhibits HDAC activity similarly in all the breast cancer cell lines with mean IC50 of 2.4 nM (range, 0.6-2.6 nM), and results in pronounced histone H4 hyperacetylation. Unlike Trapoxin (TPX) and Chlamydocin which potently inhibit HDAC1 or HDAC4 but not HDAC6, Trichostatin A inhibits these HDACs to a similar extent with IC50 of 6 nM, 38 nM, and 8.6 nM, respectively. Trichostatin A (100 ng/mL) treatment induces the expression of transforming growth factor β type II receptor (TβRII) in MIA PaCa-2 cells through the recruitment of p300 and PCAF into a Sp1-NF-Y HDAC complex that binds the DNA element of TβRII promoter, which is associated with a concomitant acetylation of Sp1 an