三氧化二砷抗肿瘤作用机制研究进展  

Advances in the research of chemotherapeutic mechanism of arsenic trioxide

作　　者：熊慧瑜[1] 符立梧[1] 

机构地区：[1]中山大学肿瘤防治中心抗癌药物研究室,广州510060

出　　处：《中国新药杂志》2003年第8期599-603,共5页Chinese Journal of New Drugs

基　　金：国家自然科学基金 (3 980 0 182 )

摘　　要：三氧化二砷 (As2 O3 )于 1999年正式通过了国家药品监督管理局的审批 ,并于 2 0 0 0年 9月 2 5日作为治疗急性早幼粒细胞白血病 (APL)的新药通过FDA的审批。As2 O3 的作用机制十分复杂 ,主要有 :降解PML RARα蛋白 ;调节凋亡相关基因Fas/Fas L ,Bcl 2 ,P53 等的表达 ;通过线粒体依赖途径诱导细胞凋亡 ;诱导肿瘤细胞分化成熟 ;通过原浆毒与过氧化自由基发挥抗肿瘤作用 ;直接损害DNA ;下调端粒酶的活性和影响血管生成等作用。Arsenic trioxide (As_2O_3),as an anticancer drug for the treatment of acute promyelocytic leukemia (APL),was approved by SDA of China in 1999 and by FDA of USA in 2000.Its mechanisms of chemotherapeutic effects were very complex.The effect of As_2O_3 has been shown to be related to down-regulation of the expression of APL-specific PML-RARα oncoprotein,down/up-regulation of the expression of apoptotic associated genes such as Fas/Fas-L,Bcl-2 and P_ 53 ,induction of mitochondrial-dependent apoptosis,induction of tumor cell differentiation,modulation of the glutathione redox system and peroxylradicals,direct damage of DNA,down-regulation of telomerase activity and inhibition of angiogenesis.

关 键 词：三氧化二砷 急性早幼粒细胞白血病 细胞凋亡 细胞分化 

分 类 号：R979.1[医药卫生—药品]