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姜黄素下调Cdc25c、CDK1和细胞周期蛋白B1并上调Wee1可促进人结肠癌Colo 205细胞进入细胞周期的G2/M期。

Down-regulation of Cdc25c, CDK1 and Cyclin B1 and Up-regulation of Wee1 by Curcumin Promotes Human Colon Cancer Colo 205 Cell Entry into G2/M-phase of Cell Cycle.

作者信息

Su Chin-Cheng, Lin Jaung-Geng, Chen Guang-Wei, Lin Wen-Chuan, Chung Jing-Gung

机构信息

School of Chinese Medicine, China Medical University, Taichung City 404, Taiwan, R.O.C.

Department of Pharmacology, China Medical University, Taichung City 404, Taiwan, R.O.C.

出版信息

Cancer Genomics Proteomics. 2006 Jan-Feb;3(1):55-61. Epub 2006 Jan 1.

PMID:31394642
Abstract

BACKGROUND

Curcumin (diferuloylmethane) exhibited potent inhibitory activities against proliferation and induced apoptosis in several tumor cell lines. It was recently reported that curcumin induced cell cycle arrest in several human cancer cell lines. However, the exact mechanisms are unclear.

MATERIALS AND METHODS

Flow cytometry was used to analyze the cell cycle in human colon cancer colo 205 cells treated with various concentrations of curcumin for 48 h. In order to further understand the mechanism of curcumin-induced G2/M arrest, the checkpoint associated with enzymes of the cell cycle were also investigated by Western blotting methods.

RESULTS

Curcumin induced G2/M arrest in the examined cells and these effects were dose- and time-dependent. Futhermore, curcumin induced Wee1 expression and decreased the Cdc25c, cyclin B1 and CDK1 expressions, resulting in the induction of G2/M cell cycle arrest in the colo 205 cells. The cDNA microarray assay was also employed to confirm gene expressions (mRNA Wee1, Cdc25c, cyclin B1 and CDK1).

CONCLUSION

The results indicate that curcumin promoted the gene expression of Wee1 and inhibited that of Cdc25c, CDK1 and cyclin B1.

摘要

背景

姜黄素(二阿魏酰甲烷)在多种肿瘤细胞系中表现出对增殖的强大抑制活性并诱导细胞凋亡。最近有报道称姜黄素在多种人类癌细胞系中诱导细胞周期停滞。然而,确切机制尚不清楚。

材料与方法

采用流式细胞术分析用不同浓度姜黄素处理48小时的人结肠癌colo 205细胞的细胞周期。为了进一步了解姜黄素诱导G2/M期停滞的机制,还通过蛋白质印迹法研究了与细胞周期酶相关的检查点。

结果

姜黄素在受试细胞中诱导G2/M期停滞,且这些作用呈剂量和时间依赖性。此外,姜黄素诱导Wee1表达并降低Cdc25c、细胞周期蛋白B1和CDK1的表达,从而导致colo 205细胞中G2/M期细胞周期停滞。还采用cDNA微阵列分析来确认基因表达(mRNA Wee1、Cdc25c、细胞周期蛋白B1和CDK1)。

结论

结果表明姜黄素促进Wee1基因表达并抑制Cdc25c、CDK1和细胞周期蛋白B1的基因表达。

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