摘要
Smac是一种线粒体促凋亡蛋白,在细胞受到凋亡刺激时,从线粒体释放到细胞质,与凋亡抑制蛋白(IAPs)特异性结合,解除IAPs对半胱氨酸天冬酶(Caspase3,7,9)的抑制作用,促进细胞凋亡。Smac在肿瘤组织中存在不同程度的缺失或释放障碍,与肿瘤的发生、发展、预后密切相关,可能成为监测肿瘤进展的分子标志物之一。利用基因技术手段将Smac基因或Smac衍生的小分子类似物导入肿瘤细胞,可减少细胞对化疗的耐药性,提高对放疗的敏感性,有望开辟肿瘤治疗的新途径。本文就Smac的结构、促凋亡作用机制、组织分布及其在肿瘤治疗中的作用作一综述。
Smac is a mitochondrial protein that interacts with inhibitor of apoptosis proteins (IAPs). Upon apoptotic stimuli, the Smac is released into the cytoplasm to inhibit the capase-binding activity of IAPs. The low expression of Smac in tissues has been reported existing in various cancers. Smac plays key roles in prognosis and chemoradiothera- py resistance of malignant tumor besides neoplasm genesis and growth. Furthermore, Smac may be a molecular ther- apeutic target in cancer patients. Overexpression of Smac by transfecting extrinsic Smac gene or Smac mimetic into tumor cell can improve their sensitivity to radiotherapy and chemotherapy, which has great significance to the treat ment of tumor. Our review will focus on the roles of Smac in structure, pro-apoptotic mechanism, tissue distribution and cancer treatment.
出处
《生物医学工程学杂志》
EI
CAS
CSCD
北大核心
2013年第3期666-669,共4页
Journal of Biomedical Engineering
基金
国家自然科学基金资助项目(81071184
30600153)