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Estrogen receptor enhances the anti proliferative effects of trichostatin a and HC-toxin in human breast cancer cells
- Estrogen receptor enhances the anti proliferative effects of trichostatin a and HC-toxin in human breast cancer cells
- Min, KN; Cho, MJ; Kim, DK; Sheen, YY
- Ewha Authors
- 신윤용; 김대기
- SCOPUS Author ID
- 신윤용; 김대기
- Issue Date
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- vol. 27, no. 5, pp. 554 - 561
- MCF-7; MDA-MB-468; human breast cancer cell; estrogen receptor; trichostatin A; HC-toxin; HDAC
- PHARMACEUTICAL SOCIETY KOREA
- SCIE; SCOPUS; KCI
- 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 anti proliferative 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 G(2)/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.
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