Heat shock protein 90 inhibitor, 17-DMAG, suppresses proliferation and induces apoptosis in pancreatic cancer cells in vitro

赖明广; 姚君; 王立生

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Heat shock protein 90 inhibitor, 17-DMAG, suppresses proliferation and induces apoptosis in pancreatic cancer cells in vitro

更新时间：2026-01-09

- Heat shock protein 90 inhibitor, 17-DMAG, suppresses proliferation and induces apoptosis in pancreatic cancer cells in vitro
- Journal of Army Medical University Vol. 35, Issue 7, Pages: 627-629(2013)
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  CLC： R73-361;R735.9;R979.14
- Published：2013
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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.
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. DOI：

　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. DOI：

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(P0.05)， 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(P0.05)。17-DMAG处理组48 h时较对照组能显著地抑制PANC-1细胞增殖(P0.05)，细胞凋亡率[（22.4±2.4）%]较对照组[(4.2±1.7)%]显著增加(P0.05)；线粒体电位显著降低(P0.05)。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 (P0.05)

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 (P0.05). After 17-DMAG treatment for 48 h

the proliferation was obviously inhibited in 17-DMAG group than in control group (P0.05)

with its apoptotic rate significantly higher [(22.4±2.4)% vs (4.2±1.7)%

P0.05]

and the mitochondrial membrane potential significantly decreased (P0.05). 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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