全反式维甲酸在卵巢癌细胞HO8910增殖中的作用
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R392.1

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The Effect of all-trans retinoic acid in the Proliferation of Human Ovarian Cancer Cells HO8910
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    摘要:

    目的: 探讨全反式维甲酸在人卵巢癌细胞生长和增殖中的作用机制。方法: 选用人卵巢癌细胞株HO8910在体外进行培养,培养时添加不同浓度的全反式维甲酸(all-trans retinoic acid ,ATRA),作用24h、48h、72h后,采用MTT比色法测定细胞生长抑制率;采用流式细胞术(flow cytometry,FCM)进行细胞周期分析;采用逆转录多聚酶链反应(reverse transcription polymerase chain reaction,RT-PCR)检测维甲酸α受体(retinoic acid receptor α ,RARα)mRNA的表达。结果: 不同浓度的全反式维甲酸对HO8910细胞生长均起到抑制作用(P<0.05),并呈浓度和时间依赖关系;能够增加G1 期细胞比例,同时降低S、G2/M 期细胞比例(P<0.05),细胞增殖指数PI﹡(P<0.05) 降低 ;能够上调维甲酸α受体mRNA的表达(P<0.05), 从而抑制卵巢癌细胞增殖。结论: 全反式维甲酸对卵巢癌细胞HO8910的增殖具有显著的抑制作用,其机制可能是通过上调维甲酸α受体mRNA的表达来实现的。

    Abstract:

    Purpose To study the effect of all-trans retinoic acid (ATRA) in the proliferation of human ovarian cancer cells. Methods HO8910 human ovarian cancer cell lines were cultured in vitro and treated with different concentrations of all-trans retinoic acid for 1, 2 or 3 days. Cell proliferation was evaluated by MTT assay.Cell cycle was analayzed by flow cytometry (FCM). The expression of retinoic acid receptor α mRNA was detected by reverse transcription- polymerase chain reaction (RT-PCR). Results Different concentrations of all-trans retinoic acid could inhibit the growth of HO8910 cells(P<0.05) in a time and dose-dependent manner.All-trans retinoic acid increased the rates of G1 and decreased the rates of S and G2/M(P< 0.05), and therefore,it decreased cells proliferation index (PI﹡)(P<0.05).It could up-regulate the expression of retinoic acid receptor α mRNA(P<0.05),then inhibit proliferation of HO8910 cells. Conclusion All-trans retinoic acid could inhibit the proliferation of human ovarian cancer cells HO8910,the molecular basis may be associated with the up-regulated mRNA of retinoic acid receptor α .

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薛昕. 全反式维甲酸在卵巢癌细胞HO8910增殖中的作用[J]. 科学技术与工程, 2010, (8): .
Xue Xin. The Effect of all-trans retinoic acid in the Proliferation of Human Ovarian Cancer Cells HO8910[J]. Science Technology and Engineering,2010,(8).

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  • 收稿日期:2009-12-17
  • 最后修改日期:2009-12-26
  • 录用日期:2009-12-23
  • 在线发布日期: 2010-03-19
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