bak基因过表达对阿霉素杀伤诱导EJ细胞凋亡的增敏作用

目的目的：探讨bak基因过度表达在膀胱癌EJ细胞凋亡途径中的作用以及对阿霉素的可能的增敏作用，并研究其作用机制。方法用脂质体法，膀胱癌细胞中转入bak／pcDNA3的设为实验组，空转pcDNA3的设为对照组，用原位杂交法检测bak在癌细胞中的表达，同时用阿霉素处理后，利用MTT法测出细胞生存率，进而用荧光分光光度计检测细胞内阿霉素的聚集量。比色法检测癌细胞内Caspase-3活性改变。结果脂质体法转基因后，bak的mRNA呈阳性表达，细胞生存率较对照组明显降低（P〈O．05）。癌细胞Caspase-3活性增强（P〈O．05），细胞内阿霉素聚集量元明显增加（P〉O．05）。结论bak基因对阿霉素杀伤膀胱癌细胞具有增敏作用，但并非通过帮助阿霉索进入细胞发挥作用，其作用机制与激活Caspase-3有关。

Sensitization of Bak Gene Cooperating with Adriamyin to Kill Drug-Resistant Bladder Cancer Cells

Objective To study the effect of gene bak at hyper-expression on bladder cancer cells and sensitization of bak gene cooperating with adriamycin.Methods Bak gene was transfected into bladder cancer cells by liposome.The expressions of bak gene were detected by in situ hybridization.The survival rate was worked out by MTT after adriamycin was added and calculated IC50 and resistant factor.The accumulation of adriamycin in the cells were examined by spectrofluorimetry.Cellular caspase-3 activities were observed by colorimetric method.Results The expression of bak mRNA was positive in EJ/bak cells.The survival rate of EJ/bak cells was significantly decreased copmared with the cells added adriamycin(P<0.05).The accumulation of adriamycin in the cells did not increase significantly.The cellular caspase-3 activities were enhanced by 4.40 times(P<0.05).Conclusion The use of bak gene and adriamycin could be more efficient to kill bladder cancer cells.But bak gene may not operate through helping adriamycin into cells.Its mechanisms might be activating caspase-3.