地西他宾诱导睾丸畸胎瘤细胞F9凋亡及机制研究

Investigation on the Mechanisms of Testicular Teratoma Cell Line F9 Apoptosis Induced by Decitabine

通过研究地西他宾对睾丸畸胎瘤细胞系F9的潜在影响及相关机制,探讨地西他宾对男性生殖系统肿瘤潜在的抗肿瘤作用.结果显示,地西他宾处理后的F9细胞增殖能力明显降低(P<0.05),且呈浓度依赖性;实验组凋亡细胞群(54.12%±16.73%)较对照组(3.21%±1.02%)明显增加(P<0.05);实验组F9细胞Bcl-2的表达较对照组明显降低,Caspas-3和Bad蛋白的表达明显增强(P<0.05);实验组F9细胞胞浆内H2O2的水平(108.35±13.05)较对照组(18.21±6.56)明显增加(P<0.01).综上,地西他宾能够体外诱导小鼠睾丸畸胎瘤细胞F9发生凋亡,其机制与提高胞浆内氧化自由基H2O2水平并进一步启动内外源性细胞凋亡信号通路有关.

Testicular teratoma is one of the common tumor types in male reproductive system. Previous report showed that decitabine had potential anti-cancer effects in various tissues. Our study aimed to explore the effects of decitabine on testicular teratoma F9 cell line as well as the related mechanisms; It will uncover the potential antitumor effects of decitabine on various tumors in reproductive system. It showed that the proliferation of F9 cells was inhibited by decitabine treatment in a dose-dependent manner, P〈0. 05）. The apoptotic rate of F9 cells in deciatbine-treated group（54. 12%±16. 73%）are much more than that in control group（3. 21%±1.02%）（ P 〈0.05）. The expression of Bcl-2 in deciatbine-treated group are less than that in control group. Whereas the expression of Bad and Caspase-3 in deciatbine-treated group are more higher than that in control group（ P〈0. 05）. Furthermore,the intracellular level of H2O2 in deciatbine-treated group（108. 35±13.05）are more higher than that in control group（18.21±6.56）（ P 〈0.01）. These data indicated that Decitabine induced testicular teratoma F9 cell line apoptosis through regulating the intrinsic and extrinsic apoptosis pathway,which is involved in the intracellular H2O2 level elevation.