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转bak基因协同阿霉素杀伤膀胱癌耐药细胞 被引量:1

Bak gene cooperating with adriamycin to kill drug-resistant bladder cancer cells
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摘要 目的 :研究转 bak基因与阿霉素 (ADM)联合杀伤膀胱癌耐药细胞的效果 ,并探讨其机制。方法 :利用脂质体将基因 bak导入膀胱癌耐药细胞 ,通过原位杂交法检测 bak m RNA的表达 ,同时加入 ADM,利用 MTT法算出细胞生存率 ,进而推算半数抑制浓度 (IC50 )和抗药指数。用荧光分光光度计检测细胞内 ADM的聚集量。结果 :转基因后 ,细胞内 bak m RNA阳性表达、细胞生存率较单用 ADM明显降低 (P<0 .0 5 ) ,细胞内 ADM聚集量无明显增加 (P >0 .0 5 )。结论 :转 bak基因可以协同 ADM更有效地杀伤膀胱癌耐药细胞 ,但并非通过帮助 ADM进入细胞起作用。 Purpose:To study the effects of killing drug resistant bladder cancer cells by the use of transferred bak gene and adriamycin and illustrate its mechanisms.Methods:Bak gene was transfected into drug resistant bladder cancer cells by liposome. The expressions of bak and bcl 2 were detected by in situ hybridization. The survival rate was worked out by MTT after adriamycin was added in and IC 50 and resistant factor were calculated. The accumulation of adriamycin in the cells were examined by spectrofluorometry.Results:The expression of bak mRNA was positive in EJ/bak cells. The survival rate of EJ/bak cells was significantly decreased compared with the cells in which adriamycin was added (P< 0.05 ). The accumulation of adriamycin in the cells did not increase significantly.Conclusions:The use of transferred bak gene and adriamycin could kill drug resisant bladder cancer cells more efficiently. But bak gene did not operate through helping adriamycin into cells.
出处 《临床泌尿外科杂志》 2001年第9期415-416,共2页 Journal of Clinical Urology
关键词 BAK基因 阿霉素 膀胱癌 多药耐药性 基因治疗 Bak genes Adriamycin Bladder cancer Multidrug resisant Gene transfer
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  • 1Ling V,Cancer,1992年,69卷,2603页
  • 2李锡明,中国药学杂志,1991年,26卷,655页
  • 3邵宁生,兰州医学院学报,1990年,16卷,78页
  • 4俞莉章,中华泌尿外科杂志,1989年,10卷,131页
  • 5鄂征,组织培养技术,1987年,100页

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  • 1Nicholson DW, Thornberry NA. Apoptosis. Life and death decisions. Science, 2003,299(5604) :214-215.
  • 2Kiefer MC, Brauer MJ, Powers VC,et al. Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak. Nature, 1995,374(6524): 736-739.
  • 3Krajewski S, Krajewska M, Reed JC.Immunohistochemical analysis of in vivo patterns of Bak expression, a proapoptotic member of the Bcl-2 protein family. Cancer Res, 1996, 56(12) :2849-2855.
  • 4Farrow SN, White JH, Martinou I,et al. Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K. Nature, 1995,374(6524):731-733.
  • 5Chittenden T, Harrington EA, O'Connor R, et al. Induction of apoptosis by the Bcl-2 homologue Bak. Nature, 1995,374 (6524):733-736.
  • 6Sattler M, Liang H, Nettesheim D, et al. Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis. Science, 1997,275(5302): 983-986.
  • 7Orth K, Dixit VM. Bik and Bak induce apoptosis downstream of CrmA but upstream of inhibitor of apoptosis. J Biol Chem, 1997,272(14):8841-8844.
  • 8Chiou SK, Tseng CC, Rao L, et al. Functional complementation of the adenovirus E1B 19-kilodalton protein with Bcl-2 in the inhibition of apoptosis in infected cells. J Virol, 1994,68(10):6553-6566.
  • 9Pataer A, Smythe WR, Yu R, et al. Adenovirus-mediated Bak gene transfer induces apoptosis in mesothelioma cell lines. J Thorac Cardiovasc Surg, 2001,121 ( 1 ) :61-67.
  • 10Stayrook KR, McKinzie JH, Burke YD,et al. Induction of the apoptosis-promoting protein Bak by perillyl alcohol in pancreatic ductal adenocarcinoma relative to untransformed ductal epithelial cells. Carcinogenesis, 1997,18(8): 1655-1658.

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