Antiproliferative effect of trichostatin A and HC-toxin in T47D human breast cancer cells.
Histone deacetylase inhibitors are new class of chemotherapeutic drugs able to induce tumor cell apoptosis and/or cell cycle arrest. Trichostatin A, an antifungal antibiotic, and HC-toxin are potent and specific inhibitors of histone deacetylase activity. In this study, we have examined the antiproliferative activities of trichostatin A and HC-toxin in estrogen receptor positive human breast cancer, T47D cells. Both trichostatin A and HC-toxin showed potent antiproliferative efficacy and cell cycle arrest at G2/M in T47D human breast cancer cells in a dose-dependent manner. Trichostatin A caused potent apoptosis of T47D human breast cancer cells and trichostatin A-induced apoptosis might be involved in an increase of caspase-3/7 activity. HC-toxin evoked apoptosis of T47D cells and HC-toxin induced apoptosis might not be mediated through direct increase in caspase-3/7 activity. We have identified potent activities of antiproliferation, apoptosis, and cell cycle arrest of trichostatin A and HC-toxin in estrogen receptor positive human breast cancer cell line T47D.[1]References
- Antiproliferative effect of trichostatin A and HC-toxin in T47D human breast cancer cells. Joung, K.E., Kim, D.K., Sheen, Y.Y. Arch. Pharm. Res. (2004) [Pubmed]
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