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全反式维甲酸在卵巢癌细胞HO8910增殖中的作用 被引量:1

The Effect of All-trans Retinoic Acid in the Proliferation of Human Ovarian Cancer Cells HO8910
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摘要 为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,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 polymerasechain reaction,RT-PCR)检测维甲酸α受体(retinoic acid receptorα,RARα)mRNA的表达。结果是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。说明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。 To study the effect of all-trans retinoic acid (ATRA) in the proliferation of human ovarian cancer cells, 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). It is resulted that different concentrations of all-trans retinoicacid could inhibit the growth of HO8910 cells (P 〈 0.05 ) in a time and dose-dependent manner. All-trans retinoic acid increases the rates of G1 and decreases the rates of S and G2/M (P 〈 0.05 ), and therefore, it decreases 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. It is conclused that 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.
出处 《科学技术与工程》 2010年第8期1844-1847,1852,共5页 Science Technology and Engineering
关键词 全反式维甲酸 维甲酸α受体 细胞周期 all-trans retinoic acid (ATRA) retinoic acid receptor α cell cycle
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  • 1Esdar C, Milasta S, Maclicke A, et al. Differentiation-associatal apoptosis of neural stem cells is effected by Bcl-2 over expression : impact on cell lineage determination. Eur J CellBiol,2001 ;80( 8 ) :539-553.
  • 2Xu X C ,Liu X,Tahara E,et al. Expression and up-regulation of retinoic acid retinoic acid reeeptor-bete is associated with retinoid sensitivity and colony formation in esophageal cancer cell lines. Cancer Res, 1999 ;59 (10) :2477-2483.
  • 3Zhao X, Demary K, Wong L,et al. Retinoic acid receptor-independent mechanism of apoptosis of melanoma cells by the retinoid CD437 (AHPN). Cell Death Differ,2001 ;8(9) :878-886.
  • 4Estey E, Koller C,Tsimberidou A M, et al. Potential curability of newly diagnosed acute promyelocytic leukemia without use of chemotherapy:The example of liposomal all-trans retinoic acid. Blood ,2005 ;105 (3) :1366-1367.
  • 5Testi A M, Biondi A, Lo Coco F, et al. GIMEMA-AIEOPAIDA protocol for the treatment of newly diagnosed acute promyelocytic leukemia (APL) in children. Blood,2005 ; 106(2 ) :447-453.
  • 6Chung J, Liu C, Smith DE, et al. Restoration of retinoic acid concentration suppresses ethanolenhanced c-Jun expression and hepatocyte proliferation in rat liver. Carcinogenesis ,2001 ;22 ( 8 ) : 1213-1219.
  • 7Rexer B N ,Zheng W L, Ong D E. Retinoic acid biosynthesis by normal human breast epithelium is via aldehyde dehydrogenase 6, absent in MCF-7cells. Cancer Res,2001 ;61 ( 19 ) :7065-7070.
  • 8Kaiser PC, Korner M, Kappeler A,et al. Retinoid receptors in ovarian cancer: expression and prognosis. Ann Oncol, 2005; 16 (9) : 1477-1487.
  • 9连利娟.林巧稚妇科肿瘤学.第3版.北京:北京人民卫生出版社,2002:405.
  • 10Varedi M, Greeley G H, Hemdon D N, et al. A thermal injury-induced circulating factor(s) compromises intestinal cell morphology, proliferation, and migration. Am J Physiol, 1999; 277 ( 1pt1 ): G175-182.

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