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

doi:10.1007/bf02980131

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

Department of Pharmaceutical Sciences

Research output: Contribution to journal › Article › peer-review

9 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 language	English
Pages (from-to)	554-561
Number of pages	8
Journal	Archives of Pharmacal Research
Volume	27
Issue number	5
DOIs	https://doi.org/10.1007/bf02980131
State	Published - 31 May 2004

Bibliographical note

Funding Information:
This research was supported by the grant NTP 238 from the KFDA of Korea.

Keywords

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/bf02980131

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@article{dba63eaa66e24a7d83020b142ec59115,

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

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.",

keywords = "Estrogen receptor, HC-toxin, HDAC, Human breast cancer cell, MCF-7, MDA-MB-468, Trichostatin A",

author = "Kyung, \{Nan Min\} and Min, \{Jung Cho\} and Kim, \{Dae Kee\} and Sheen, \{Yhun Yhong\}",

note = "Funding Information: This research was supported by the grant NTP 238 from the KFDA of Korea.",

year = "2004",

month = may,

day = "31",

doi = "10.1007/bf02980131",

language = "English",

volume = "27",

pages = "554--561",

journal = "Archives of Pharmacal Research",

issn = "0253-6269",

publisher = "Pharmaceutical Society of Korea",

number = "5",

}

TY - JOUR

T1 - Estrogen receptor enhances the antiproliferative effects of trichostatin A and HC-toxin in human breast cancer cells

AU - Kyung, Nan Min

AU - Min, Jung Cho

AU - Kim, Dae Kee

AU - Sheen, Yhun Yhong

N1 - Funding Information: This research was supported by the grant NTP 238 from the KFDA of Korea.

PY - 2004/5/31

Y1 - 2004/5/31

N2 - 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.

AB - 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.

KW - Estrogen receptor

KW - HC-toxin

KW - HDAC

KW - Human breast cancer cell

KW - MCF-7

KW - MDA-MB-468

KW - Trichostatin A

UR - https://www.scopus.com/pages/publications/16544367723

U2 - 10.1007/bf02980131

DO - 10.1007/bf02980131

M3 - Article

C2 - 15202563

AN - SCOPUS:16544367723

SN - 0253-6269

VL - 27

SP - 554

EP - 561

JO - Archives of Pharmacal Research

JF - Archives of Pharmacal Research

IS - 5

ER -

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

Abstract

Bibliographical note

Keywords

UN SDGs

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