[1]赖明广,姚君,王立生.HSP90抑制剂17-DMAG调控胰腺癌细胞PANC-1增殖及凋亡的初步研究[J].陆军军医大学学报(原第三军医大学学报),2013,35(07):627-629.
 Lai Mingguang,Yao Jun,Wang Lisheng.Heat shock protein 90 inhibitor, 17-DMAG, suppresses proliferation and induces apoptosis in pancreatic cancer cells in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(07):627-629.
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HSP90抑制剂17-DMAG调控胰腺癌细胞PANC-1增殖及凋亡的初步研究(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
35卷
期数:
2013年第07期
页码:
627-629
栏目:
论著
出版日期:
2013-04-15

文章信息/Info

Title:
Heat shock protein 90 inhibitor, 17-DMAG, suppresses proliferation and induces apoptosis in pancreatic cancer cells in vitro
作者:
赖明广姚君王立生
暨南大学第二临床医学院消化内科
Author(s):
Lai Mingguang Yao Jun Wang Lisheng
Department of Gastroenterology, Second Clinical College, Jinan University, Shenzhen, Guangdong Province, 518020, China
关键词:
17-DMAG增殖凋亡PANC-1
Keywords:
17-DMAG proliferation apoptosis PANC-1
分类号:
R73-361; R735.9; R979.14
文献标志码:
A
摘要:
目的      探讨热休克蛋白90(HSP90)功能特异性抑制剂17-DMAG对胰腺癌细胞PANC-1增殖与凋亡的影响。      方法       体外培养腺癌细胞PANC-1, 17-DMAG处理PANC-1细胞后,CCK8法测定细胞生长曲线,观察细胞增殖的抑制情况,流式细胞仪测定细胞凋亡率的变化,Jc-l染色检测线粒体膜电位变化,RT-PCR法测定17-DMAG处理PANC-1细胞前后Bcl-2、Bax表达变化。      结果       17-DMAG处理组24 h时D(490)值较对照组差异无统计学意义(P>0.05), 48、72 h后较对照组D(490)值分别减少(18.3±2.4)%、(21.5±3.2)%,差异有统计学意义(P<0.05)。17-DMAG处理组48 h时较对照组能显著地抑制PANC-1细胞增殖(P<0.05),细胞凋亡率[(22.4±2.4)%]较对照组[(4.2±1.7)%]显著增加(P<0.05);线粒体电位显著降低(P<0.05)。RT-PCR结果显示,17-DMAG处理组抑制Bcl-2的表达,促进Bax的表达。      结论       17-DMAG可抑制胰腺癌细胞PANC-1增殖并诱导其凋亡,该效应可能是通过调控凋亡相关蛋白Bcl-2家族成员的表达实现。
Abstract:
Objective       To determine the effect of 17-dimethylaminoethylamino-17-demethoxy geldanamycin  (17-DMAG), a specific inhibitor of heat shock protein 90 (HSP90), on the proliferation and apoptosis in  pancreatic cancer cell line PANC-1.       Methods       After PANC-1 cells were treated with 17-DMAG at the final dose of 500 nmol/mL, CCK8 assay was used to plot cell growth curve. Flow cytometry was used to detect the cell cycle and apoptosis. JC-1 mitochondrial membrane potential assay kit was applied to detect mitochondrial membrane potential. Reverse transcription polymerase chain reaction (RT-PCR) was applied to detect the mRNA expression of Bcl-2 and Bax.       Results      17-DMAG treatment for 24 h resulted in no significant difference in cell growth in PANC-1 cells (P>0.05), but when the treatment was prolonged to 48 and 72 h, the growth was decreased by (18.3±2.4)% and (21.5±3.2)%, respectively (P<0.05). After 17-DMAG treatment for 48 h, the proliferation was obviously inhibited in 17-DMAG group than in control group (P<0.05), with its apoptotic rate significantly higher [(22.4±2.4)% vs (4.2±1.7)%, P<0.05], and the mitochondrial membrane potential significantly decreased (P<0.05). 17-DMAG down-regulated the mRNA level of Bcl-2, and  consequently up-regulated that of Bax in PANC-1 cells.       Conclusion      17-DMAG inhibits the proliferation and induces the apoptosis in PANC-1 cells by regulating apoptosis-related protein Bcl-2 family.

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更新日期/Last Update: 2013-04-07