Estrogen receptor enhances the antiproliferative effects of trichostatin A and HC-toxin in human breast cancer cells

Nan Min Kyung, Jung Cho Min, Dae Kee Kim, Yhun Yhong Sheen

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Trichostatin A, an antifungal antibiotics, and HC-toxin are potent and specific inhibitors of histone deacetylase activity. Histone deacetylase inhibitors are new class of chemotherapeutic drugs able to induce tumor cell apoptosis and/ or cell cycle arrest. In this study, the antiproliferative activities of trichostatin A and HC-toxin were compared between estrogen receptor positive human breast cancer cell MCF-7 and estrogen receptor negative human breast cancer cell MDA-MB-468. Trichostatin A and HC-toxin showed potent antiproliferative activity in both MCF-7 and MDA-MB-468 cells. In MCF-7 cells that contain high level estrogen receptor, trichostatin A and HC-toxin brought about three-times more potent cell growth inhibitory effect than estrogen receptor negative MDA-MB-468 cells. Both trichostatin A and HC-toxin showed cell cycle arrest at G2/M phases of MCF-7 and MDA-MB-468 cells in a dose- and time- dependent manner. Trichostatin A and HC-toxin also induced apoptosis from MCF-7 and MDA-MB-468 cells in a dose- and time-dependent manner. Results of this study suggested that antiproliferative effects of trichostatin A and HC-toxin might be involved in estrogen receptor signaling pathway, but cell cycle arrest and apoptosis of trichostatin A and HC-toxin might not be involved in estrogen receptor system of human breast cancer cells.

Original languageEnglish
Pages (from-to)554-561
Number of pages8
JournalArchives of Pharmacal Research
Volume27
Issue number5
DOIs
StatePublished - 31 May 2004

Keywords

  • Estrogen receptor
  • HC-toxin
  • HDAC
  • Human breast cancer cell
  • MCF-7
  • MDA-MB-468
  • Trichostatin A

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