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作 者:李登欣[1] 张建业[1] 张莲英[1] 何维敬[1]
机构地区:[1]山东医科大学生物化学教研室
出 处:《山东医科大学学报》1999年第2期91-93,共3页Acta Academiae Medicinae Shandong
基 金:山东省科委科研基金
摘 要:为研究VP-16对雄激素非依赖性前列腺癌细胞PC-3凋亡的诱导作用,应用HE染色观察细胞的形态学改变,以DNA凝胶电泳和流式细胞术(FCM)分析细胞凋亡和细胞周期分布,同时应用3H-TdR掺入法研究VP-16对PC-3细胞DNA合成的影响。结果表明,(1)凋亡的PC-3细胞呈明显的形态学改变;(2)DNA断裂呈梯形变化;(3)PC-3细胞凋亡率随VP-16作用浓度增加和时间延长逐渐增高;(4)VP-16能够明显抑制PC-3细胞DNA的合成。提示VP-16可诱导前列腺肿瘤细胞凋亡。To study VP16 induce apoptosis in PC3 cells, whose growth is androgen independent. The change of cell morphology was observed by HE staining, DNA gel electrophoresis and flow cytometry(FCM) were applied to investigate the apoptosis in PC3 cells and distribution of cell cycle, DNA synthesis was detected by 3KG*2]HTdR penetration. HE staining showed typical apoptotic morphological changes in PC3 cells; DNA cleavage in PC3 cell presented ladder lanes, the percentage of apoptotic cells was increased with the increasing of concentration and exposure time of VP16; DNA synthesis in PC3 cells was strongly inhibited by VP16. These findings suggest that VP16 can induce apoptosis in prostatic cancer.
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