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.