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Estrogen Receptor Enhances the Antiproliferative Effects of Trichostatin A and HC-toxin in Human Breast Cancer Cells
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  • Estrogen Receptor Enhances the Antiproliferative Effects of Trichostatin A and HC-toxin in Human Breast Cancer Cells
  • Estrogen Receptor Enhances the Antiproliferative Effects of Trichostatin A and HC-toxin in Human Breast Cancer Cells
저자명
Min. Kyung-Nan,Cho. Min-Jung,Kim. Dae-Kee,Sheen. Yhun-Yhong
간행물명
Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea
권/호정보
2004년|27권 5호|pp.554-561 (8 pages)
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

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 G$_2$/M phases of MCF-7 and MDA-MB-468 cells in a dose- and time- depen- dent 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 antipro-liferative 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.