组蛋白去乙酰酶抑制剂对结肠癌细胞增殖和ID4基因表达的影响
组蛋白去乙酰酶抑制剂;结肠癌;ID4基因,张波,陈剑英,王国斌,陈道达,张波,通讯作者:,EffectsofhistonedeacetylaseinhibitoroncoloncancercellgrowthandID4geneex
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张波, 陈剑英, 王国斌, 陈道达, 华中科技大学同济医学院附属协和医院普外科 湖北省武汉市 430022
张波, 2003年华中科技大学附属协和医院医学博士, 主治医生, 主要从事结直肠癌和乳腺癌的分子标志物研究.
通讯作者: 张波, 430022, 湖北省武汉市解放大道1277号, 华中科技大学同济医学院附属协和医院普外科.
unionzhang@yahoo.com
电话: 027-85726494 传真: 027-85756343
收稿日期: 2007-03-30 接受日期: 2007-04-17
Effects of histone deacetylase inhibitor on colon cancer cell growth and ID4 gene expression
Bo Zhang, Jian-Ying Chen, Guo-Bin Wang, Dao-Da Chen
Bo Zhang, Jian-Ying Chen, Guo-Bin Wang, Dao-Da Chen,Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, Hubei Province, China
Correspondence to:Dr. Bo Zhang, Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, Hubei Province, China. unionzhang@yahoo.com
Received:2007-03-30 Accepted:2007-04-17
Abstract
AIM: To investigate whether Trichostatin A (TSA) possesses anti-tumor activity against human colon cancer cells.
METHODS: The human colon cancer cell line Caco2 was treated with different concentrations of TSA, a potent and specific histone deacetylase inhibitor, for 0 to 5 d. The growth of Caco2 cells was observed by MTT assay before and after TSA treatment. The Caco2 cell cycle was analyzed by flow cytometry. The expression of ID4 mRNA was observed by reverse transcription-polymerase chain reaction.
RESULTS: Trichostatin A in a dose-dependent fashion significantly inhibited the proliferation of colon cancer cells at 100 μg/L (P < 0.05). The inhibition rate increased sharply from day 3 to 5 (57.3% to 70.2%). TSA treatment induced cell cycle arrest at the G1 phase but did not increase apoptotic cell death as shown by flow cytometry. ID4 mRNA was expressed in Caco2 cells after 20 μg/L TSA treatment, but it was only weakly detectable before treatment.
CONCLUSION: Our results demonstrated that TSA inhibited colon cancer cell growth in vitro, possibly through G1 cell cycle arrest and re-expression of the ID4 gene ......
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