维普中文期刊产品整合服务

组织因子/因子VII激活PI3K/Akt信号途径调控阿霉素诱导人胶质母细胞瘤细胞凋亡的研究(英文)

查看全文 作　　者：Hao [1]Tang;Jun [2]Fang;Kai [1]Shu;Muxiang [3]Zhou;Shanjun [2]Song;Ling [1]Li;Ting [1]Lei 高影响力作者 机构地区：[1]Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;[2]Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China;[3]Division of Pediatric Hematology/Oncology, Emory University School of Medicine, Atlanta 30322, USA高影响力机构 出　　处：《The Chinese-German Journal of Clinical Oncology》索引2007年第6卷第5期,共5页高影响力期刊 摘　　要：Objective: To investigate the role of tissue factor (TF) in chemotherapeutic reagent - induced apoptosis on human glioblastoma and explore its mechanism. Methods: The expression of TF was examined by Western blotting. The cytotoxicity of doxorubicin was determined by WST assay. The activation of Caspase-3 and PARP induced by adoxorubicin were tested by Western blotting. Results: Human glioblastoma cell line U373MG expressed high level of TF while LN-229 was with low-TF level. The chemotherapeutic reagent doxorubicin revealed stronger cytotoxic effect on high-TF U373MG cells than low-TF LN-229 cells. Enforced strong expression of TF was achieved by transfection of TF-pcDNA3 combinant on LN-229 cells in a dose-dependent manner. Enforced TF expression in transfected LN-229 cells not only impaired the doxorubicin-induced cleavage of Caspase-3 and PARP, but also inhibited the cytotoxic effect of doxorubicin. Furthermore, activation of Akt was strong in high-TF U373MG cells but weak in low-TF LN-229 cells. Incubation of factor VII (FVII) with enforced TF-expressing LN-229 cells increased the phosphorylation of Akt in a time-dependent manner. Conclusion: These results suggest that over-expression of TF on glioblastoma could inhibit doxorubicin-induced apoptosis. Interaction of FVII and TF activates the downstream PI3K/Akt pathway. Tumor-derived over-expression of TF might play a role in chemotherapy resistance in glioblastoma, at lest in part, by activating PI3K/Akt-mediated survival and anti-apoptotic mechanism through the interaction of TF/FVII signaling. 关 键 词：组织因子 信号途径 调控 阿霉素 人胶质母细胞瘤 细胞凋亡
相关文献

参考文献(23)

耦合文献(9)

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1　渝公网安备 50019002500403号　违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费