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PPARγ激动剂罗格列酮诱导人前列腺癌细胞系LNCAP凋亡的作用

The Effects of PPAR Agonist Rosiglitazone on Proliferation and Apoptosis in Human Prostate Adenocarcinoma Cell Line LNCAP
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摘要 目的:探讨罗格列酮(ROZ)对体外培养细胞系LNCAP增殖及凋亡的作用。方法:20、50、100μmol/LROZ作用LNCAP细胞24h、48h、72h后,MTT法检测R0Z对LNCAP细胞生长的影响。采用末端脱氧核苷酸转移酶原位标记(TUNEL法)和流式细胞术检测细胞凋亡情况。Western Blot检测LNCAP细胞中Casepase-3表达水平的变化。结果:ROZ(20μmol/L至100μmol/L)对前列腺癌细胞有显著的增殖抑制作用,以100μmol/L浓度最为明显。ROZ(100μmol/L)作用72h后最高增殖抑制率达78.58%。流式细胞仪检测结果显示,LNCAP细胞凋亡数目随药物浓度的增加呈递增趋势;100μmol/LROZ作用72h后凋亡细胞数达48.11%。与此一致,TUNEL染色阳性细胞数目在ROZ处理组显著增多,WesternBlot检测显示,ROZ显著增加LNCAP细胞中Caspase-3蛋白表达水平。结论:ROZ在体外对前列腺癌细胞系LNCAP有明显的增殖抑制及促进凋亡作用,有望成为前列腺癌患者新的治疗方法。 Objective:To investigate the effects of Rosiglitazone on proliferation and apoptosis of human prostate adenocarcinoma cell line LNCAP in vitro. Methods:After LNCAP cells were treated with ROZ for 24, 48, 72 hours, MTT assay was used to detect the changes in growth LNCAP. LNCAP cell apoptosis was evaluated by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The expression levels of Caspase-3 were examined in LNCAP cells by Western Blot. Results:ROZ significantly inhibited cell growth of LNCAP cells. At the concentration of 100 mol/L, ROZ showed a high inhibitory rate of 78.58 % after 72 h treatment. Flow cytomewtry showed a significant increase in the number of apoptosis cells, and it reached 48.11% after ROZ (100 mol/L) treatment for 72 h. At the same time, TUNEL staining positive cells significantly increased in ROZ treated group compared to the control. Western Blot showed that ROZ enhanced the expression of Caspase-3, a critical protein inducing cell apoptosis. Conclusions : Rosiglitazone inhibits cell growth of human prostate adenocarcinoma cell line LNCAP by inducing cell apoptosis in vitro. ROZ might become a new drug to treat patients with prostate cancer.
出处 《现代生物医学进展》 CAS 2009年第7期1253-1255,共3页 Progress in Modern Biomedicine
关键词 罗格列酮 前列腺癌 LNCAP 凋亡 Rosiglitazone Prostate cancer LNCAP Apoptosis
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  • 1Mettlin C J, Murphy G. The national cancer data base report on cancer [J]. Cancer,1994, 74(5): 1640-1648 被引量:1
  • 2Issemann I, Green S. Activation of a member of the steroid hormone receptor super family by peroxisome proliferators [J]. Nature, 1990, 347(6294): 645-650 被引量:1
  • 3Koeffier HP. Peroxisome proliferator-activated receptor gamma and cancers [J]. Clin Cancer Res, 2003, 1(9): 1-9 被引量:1
  • 4Zander T, Kraus J A,Grommes C, et al.Induction of apoptosis in human and rat glioma by agonists of the nuclear receptor PPARgamma [J]. J Neurochem, 2002, 81(5): 1052-1060 被引量:1
  • 5Farrow B, Evers BM. Activation of PPAR gamma increases PTEN expression in pancreatic cancer cells [J]. Biochem Biophys Res Commun, 2003, 301(1): 50 被引量:1
  • 6Mueller E, Smith M, Sarraf P ,et al. Effects of ligand activation of peroxisome proliferator-activated receptor gamma in human prostate cancer [J]. Proc Nat Acad Sci USA, 2000, 97:10990-10995 被引量:1
  • 7Kerr JF. Shrinkage necrosis: a distinct mode of cellular death [J]. J Parhol, 1971, 105(1): 15-20 被引量:1
  • 8SmithMRKantoftPW.Peroxisomeproliferator-activatedreceptorgamma (PPargamma) as a novel target for prostate cancer [J]. InvestNew Drugs, 2002, 20(2): 195-200 被引量:1
  • 9Kitamura S, Miyazaki Y, Shinomura Y, et al. Peroxisome proliferator-activated receptor gamma induces growth arrest and differentiation markers of human colon cancer cells [J]. Jpn J Cancer Res, 1999,90(1): 75-80 被引量:1

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