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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。
Objective To investigate the effect of 17-DMAG, a specific inhibitor of heat shock protein 90 (HSP90) on the proliferation and apoptosis of pancreatic cancer cell line PANC-1. Methods PANC-1 cells were treated with PANC-1,17-DMAG in vitro and the cell growth curve was determined by CCK8 assay. The inhibition of cell proliferation was observed by flow cytometry. The changes of apoptosis rate were determined by Jc-1 staining The change of mitochondrial membrane potential was detected. The expression of Bcl-2 and Bax in 17-DMAG-treated PANC-1 cells was detected by RT-PCR. Results Compared with the control group, the D (490) value in 17-DMAG treatment group had no significant difference (P> 0.05) at 24 h, and decreased by 18.3 ± 2.4% (21.5 ± 3.2)%, the difference was statistically significant (P <0.05). Compared with the control group, the proliferation of PANC-1 cells was significantly inhibited by 17-DMAG treatment at 48 h (P <0.05), and the apoptotic rate [(22.4 ± 2.4)%] was significantly higher than that of the control group [(4.2 ± 1.7)%] (P <0.05). The mitochondrial potential decreased significantly (P <0.05). RT-PCR results showed that 17-DMAG treatment inhibited Bcl-2 expression and promoted Bax expression. Conclusion 17-DMAG can inhibit the proliferation and induce the apoptosis of pancreatic cancer cell PANC-1, which may be through regulating the expression of Bcl-2 family member.