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机构地区:[1]黔南民族医学高等专科学校基础医学部,贵州都匀558000 [2]贵州医科大学附属医院病理科,贵州贵阳550004 [3]贵阳市第一人民医院泌尿外科,贵州贵阳550003
出 处:《中国病理生理杂志》2017年第6期1130-1133,共4页Chinese Journal of Pathophysiology
基 金:贵州省卫生厅科学技术基金项目(No.gzwkj2010-1-068)
摘 要:目的:观察白皮杉醇对前列腺癌细胞株DU145的细胞活力、迁移与侵袭能力的作用并初步讨论其机制。方法:CCK-8法检测不同浓度白皮杉醇(0、5、10、20、40和80μmol/L)作用不同时间(12、24、36和48 h)对DU145细胞活力的影响;划痕实验与Transwell小室法分别检测白皮杉醇对DU145细胞迁移与侵袭能力的影响;Western blot法检测p-JAK2与p-STAT3的蛋白水平。结果:CCK-8法结果显示白皮杉醇呈浓度依赖性抑制DU145细胞的活力;给予白皮杉醇干预后,细胞迁移数和侵袭数显著减少,p-JAK2与p-STAT3蛋白水平显著下降。结论:白皮杉醇呈浓度依赖性抑制前列腺癌细胞的生长,并具有抑制细胞迁移与侵袭的作用,其机制可能与抑制JAK2/STAT3信号通路有关。AIM : To investigate the effect of piceatannol on the viability, and the abilities of migration and in-vasion in the prostate cancer cells. ME THODS: DU145 cells were treated with piceatannol at different doses ( 0 , 5 , 10, 20, 40 and 80 jjimol/L) for different time (12, 24, 36 and 48 h) as indicated. The cell viability was assessed by CCK-8 assay. The migration and invasion abilities of the cells were analyzed by wound healing assay and Transwell assay, respec-tively. The protein levels of p-JAK2 and p-STAT3 were detected by Western blot. R ESUL TS : Piceatannol dose-dependent- ly decreased the cell viability. After treatment with piceatannol, the abilities of migration and invasion of the cells were sig-nificantly inhibited. Moreover, treatment with piceatannol resulted in marked decreases in the protein levels of p-JAK2 and p-STAT3. CONCLUSION : Piceatannol inhibits the viability, migration and invasion of the prostate cancer cells via regu-lating the JAK2/STAT3 signaling pathway.
关 键 词:白皮杉醇 细胞活力 细胞迁移 JAK2/STAT3信号通路
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