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非那雄胺抑制前列腺癌增殖的机制:一项利用cDNA微阵列的研究

[Mechanism of inhibiting the proliferation of prostate cancer by finasteride: a study using cDNA microarray].

作者信息

Chen Gang, Geng Jiang, Zhang Yuan-fang

机构信息

Department of Urology, Jinshan Hospital, Fudan University, Shanghai 200540, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2005 Jun 8;85(21):1489-92.

PMID:16061029
Abstract

OBJECTIVE

To screen the genes related to finasteride treatment that reduces the proliferation of prostate cancer cells.

METHODS

The prostate cancer cells of the line LNCaP sensitive to finasteride treatment were cultured. Finasteride was added into the culture fluid. A cDNA microarray consisting of 96 human genes was used to identify the genes showing differential expression.

RESULTS

Finasteride significantly inhibited the proliferation of the prostate cancer cells of the line LNCaP. Twenty-nine genes out of the 96 genes showed differential expression under finasteride treatment 11 were upregulated and 18 were down-regulated, including those significant in cell metabolism, proliferation, apoptosis, and cell signal transduction, such as AKR1B1, PTEN, NKX3.1, PMEPA1, PSA, and XRCC2.

CONCLUSION

Inhibiting the proliferation of prostate cancer cells by finasteride may involve the cooperative effect of multiple genes and pathways.

摘要

目的

筛选与非那雄胺治疗相关的、可降低前列腺癌细胞增殖的基因。

方法

培养对非那雄胺治疗敏感的LNCaP系前列腺癌细胞。将非那雄胺加入培养液中。使用由96个人类基因组成的cDNA微阵列来鉴定显示差异表达的基因。

结果

非那雄胺显著抑制LNCaP系前列腺癌细胞的增殖。96个基因中有29个基因在非那雄胺治疗下显示差异表达,其中11个上调,18个下调,包括在细胞代谢、增殖、凋亡和细胞信号转导方面有显著作用的基因,如AKR1B1、PTEN、NKX3.1、PMEPA1、PSA和XRCC2。

结论

非那雄胺抑制前列腺癌细胞增殖可能涉及多个基因和途径的协同作用。

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