1-(3,4-dimethoxyphenyl)-3,5-dodecenedione (I6) induces G1 arrest and apoptosis in human promyelocytic leukemia HL-60 cells.

doi:10.1016/j.leukres.2005.04.014

中山醫學大學機構典藏 CSMUIR > 健康管理學院 > 醫學應用化學系暨碩士班 > 期刊論文 > Item 310902500/3780

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/3780

Title:	1-(3,4-dimethoxyphenyl)-3,5-dodecenedione (I6) induces G1 arrest and apoptosis in human promyelocytic leukemia HL-60 cells.
Authors:	Mei-Hua Hsu;Sheng-Chu Kuo;Chun-Jen Chen;Jing-Gung Chung;Ya-Yun Lai;Li-Jiau Huang
Contributors:	中山醫學大學:應用化學系
Keywords:	1-(3,4-Dimethoxyphenyl)-3,5-dodecenedione (I6);HL-60;Cell cycle;G1 arrest;Apoptosis
Date:	2005
Issue Date:	2011-05-17T08:49:12Z (UTC)
ISSN:	0145-2126
Abstract:	1-(3,4-Dimethoxyphenyl)-3,5-dodecenedione (I6), a gingerdione derivative, was synthesized in our laboratory, has been demonstrated to be an effective anti-tumor agent in human leukemia cells. Gingerdione is one of the components from ginger. In the present study, we found that I6 could inhibit cell proliferation in the time- and dose-dependent manner in human promyelocytic leukemia HL-60 cells. To investigate the anti-proliferation mechanism of I6, cell cycle analysis was performed. Results showed that I6 induced significant G1 arrest and apoptosis in HL-60 cells. It was proved by the reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of regulatory on G1 arrest that the levels of p15 and p27 increased after treatment and mRNA levels of cyclin D2, cyclin E, and cdc25A were decreased. The I6-induced apoptosis was further confirmed by DNA fragmentation assay. The DNA gel electrophoresis showed that I6 induced DNA fragmentation, a biochemical hallmark of apoptosis, in HL-60 cells. I6-induced apoptosis was accompanied by an apparent up-regulation of caspase-3, and down-regulation of Bcl-2. Taken together, these results suggest that markedly down-regulation of G1 associated cyclin D2, cyclin E and cdc25A and up-regulation of CDKI, p15 and p27, and may contribute to I6-mediated cell cycle arrest. Furthermore, the Bcl-2 expression decrease and caspase-3 activation may be the plausible mechanism by which I6 induced apoptosis. These results suggest that I6 is a potent anti-HL-60 drug and possess a significant action on cell cycle before commitment for apoptosis occurrence.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/3780 http://dx.doi.org/10.1016/j.leukres.2005.04.014
Relation:	Leukemia Research. 29, 1399-1406.
Appears in Collections:	[醫學應用化學系暨碩士班] 期刊論文

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