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作 者:孟爱国[1] 刘春艳[1] 石峻[2] 殷华[2] 赵建
机构地区:[1]天津大学药物科学与技术学院姜申德实验室,天津300072 [2]华北煤炭医学院附属医院检验科,唐山063000 [3]开滦矿务局医院胸外科,唐山063000
出 处:《肿瘤》2007年第11期874-877,共4页Tumor
摘 要:目的:探讨过氧化物酶体激活物活化受体1(peroxisome proliferator-activated receptor gamma,PPARγ)活化在诱导人胃癌MGCS03细胞周期停滞中的作用。方法:MTT法检测吡格列酮(pioglitazone,PGZ)对MGCS03细胞增殖的抑制作用;流式细胞术检测肿瘤细胞周期的改变;RT—PCR方法检测PPARγ、细胞周期蛋白CyclinD1和细胞周期蛋白依赖性激酶CDK4的表达。结果:0.1—10μmol/L PGZ作用MGCS03细胞96h后能显著抑制细胞增殖;10μmol/LPGZ分别作用48、72和96h,G1期细胞随着作用时间的延长而增加,呈明显的G1期阻滞;在MGC803细胞中PPARγ表达较弱,经10μmol/LPGZ作用48h表达水平显著增加;作用96h,细胞中细胞周期调节因子CDK4表达显著降低(P〈0.01),CyclinD1轻微下调。结论:PPAR1活化能诱导MGC803细胞周期G1期阻滞,该作用可能与其下调细胞周期因子CDK4和CyclinD1的表达有关。Objective : To explore the effect of activation of peroxisome proliferator-activated receptor gamma (PPARγ) on cell cycle arrest of gastric carcinoma cell line MGC803. Methods:The inhibitory effect of pioglitazone (PGZ) on proliferation of MGC803 cells was analyzed by MTT assay. Cell cycle were detected by flow cytometry (FCM). The protein expression of PPARγ, cyclinD1 and cell cycle protein-dependent kinase CDK4 in MGC803 cells was determined by reverse transcriptase-polymerase chain reaction ( RT- PCR). Results: Treatment with 0.1-10 μmol/L PGZ for 96 h significantly inhibited cell proliferation. The proportion of MGC803 cells at G1 phase was significantly increased when treated with 10 μmol/L PGZ for 48, 72 and 96 h, and showed an apparent G1 phase arrest. The expression of PPARγ was at a low level in MGC803 cells and significantly up-regulated when treated with 10 μmol/L PGZ for 48 h (P 〈0.01 ). The expression of CDK4 in MGC803 cells was significantly down-regulated when treated with 10 μmol/L PGZ for 96 h (P 〈 0.01 )and the expression of cyclinD1 was slightly down-regulated. Conclusion: Activation of PPARγ significantly induces G1 phase arrest, which is associated with down-regulation of the expression of CDK4 and cyclinD1.
关 键 词:胃肿瘤 过氧化物酶体增殖物激活受体 细胞周期 MGC803细胞
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