期刊文献+

PBMC对B7-2基因修饰的肝癌细胞Bel-7402体外杀伤作用的研究

PBMC killing-effect on the B7-2 gene-modified Bel-7402 hepatoma cells in vitro
暂未订购
导出
摘要 目的研究B7-2基因修饰肿瘤后对T细胞活化的影响,探索B7-2在肿瘤免疫治疗中的作用。方法构建B7-2基因的表达载体,转染Bel-7402细胞,与外周血单核细胞(PBMC)共孵育,利用流式细胞术(FCM)检测Bel-7402细胞的凋亡。结果 B7-2基因修饰的Bel-7402细胞和PBMC细胞共培养4 h后,凋亡率为12.7%,与对照组(7.5%)比较,细胞凋亡率显著增加(P<0.01)。结论 B7-2基因修饰能够增强肿瘤细胞对淋巴细胞的活化作用,为基于B7-2的抗肿瘤治疗奠定了基础。 Objective To study the influence of B7-2 gene modified tumor cells on T cells activation,and the role of B7-2 in tumor immunotherapy,and to explore new ideas on designing the malignant tumor comprehensive treatment based on B7-2. Methods Recombinant B7-2 gene expression vector was constructed,and Bel-7402 cells were tranfected,and then co-cultured with peripheral blood mononuclear cells(PBMC),and Bel-7402 cells apoptosis were detected subsequently by flow cytometry(FCM).Results Bel-7402 cells modified by B7-2 gene were co-cultured with PBMC for 4 h,and the apoptosis rate detected by flow cytometry was 12.7%,which was significantly increased compared with that in the control group(7.5%)(P0.01).Conclusion B7-2 gene-modified tumor cells could enhance lymphocytic activation,which suggesting the feasibility of antitumor treatment based on B7-2.
出处 《广东药学院学报》 CAS 2010年第3期310-313,共4页 Academic Journal of Guangdong College of Pharmacy
基金 "重大新药创制"科技重大专项(2009ZXD9103-708) 广东省高校优秀青年创新人才培养项目(2008342) 广东药学院师资队伍建设经费
关键词 BEL-7402细胞 PBMC 流式细胞术 脂质体 凋亡 Bel-7402 cells PBMC flow cytometry liposome apoptosis
  • 相关文献

参考文献2

二级参考文献23

  • 1陈佳佳,李兰娟.B7-CD28家族共刺激途径的研究进展及其临床意义[J].国外医学(流行病学.传染病学分册),2004,31(6):334-338. 被引量:3
  • 2Hilger-Eversheim K,Moser M,Schorle H,et al.Regulatory roles of AP-2 transcription factors in vertebrate development,apoptosis and cell-cycle control.Gene,2000,260:1-12.
  • 3Wajapeyee N,Somasundaram K.Cell cycle arrest and apoptosis induction by activator protein 2alpha (AP-2alpha) and the role of p53 and p21WAF1/CIP1 in AP-2alpha-mediated growth inhibition.J Biol Chem,2003,278:52093-52101.
  • 4Zhang X,Leung YK,Ho SM.AP-2 regulates the transcription of estrogen receptor (ER)-beta by acting through a methylation hotspot of the ON promoter in prostate cancer cells.Oncogene,2007,26:7346-7354.
  • 5Zhang J,Hagopian-Donaldson S,Serbedzija G,et al.Neural tube,skeletal and body wall defects in mice lacking transcription factor AP-2.Nature,1996,381:238-241.
  • 6Kannan P,Buettner R,Chiao P J,et al.N-ras oncogene causes AP-2 transcriptional self-interference,which leads to transformation.Genes Dev,1994,8:1258-1269.
  • 7Zeng YX,Somasundaram K,el-Deiry WS.AP2 inhibits cancer call growth and activates p21WAF1/CIP1 expression.Nat Genet,1997,15:78-82.
  • 8Tummala R,Romano RA,Fuchs E,et al.Molecular cloning and characterization of AP-2 epsilon,a fifth member of the AP-2 family.Gene,2003,321:93-102.
  • 9Moser M,Pscherer A,Roth C,et al.Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2beta.Genes Dev,1997,11:1938-1948.
  • 10Gee JM,Robertson JF,Ellis IO,et al.Immunohistochemical analysis reveals a tumour suppressor-like role for the transcription factor AP-2 in invasive breast cancer.J Pathol,1999,189:514-520.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部