摘要
凋亡是细胞胞内在程序性死亡，是调节组织稳态的中心环节。肿瘤的发生以及其化疗与细胞凋亡密切相关。肿瘤化疗药物的作用机制与死亡受体（DR）介导的凋亡在不同层次存在着多重交叉点，因而探索参与DR凋亡途径的蛋白信号分子与化疗药物作用位点的潜在联系将为人类肿瘤治疗提供新的靶点和思路。
Apoptosis, the cell＇s intrinsic death program, is a key regulator of tissue homeostasis, kill- ing of cancer cells by chemotherapy is predominantly mediated by triggering apoptosis in target cells. As the classic apoptosis-pathway, Fas/Fas-ligand and TNF-receptor/TNF play important roles in anti-cancer therapy. Tumor necrosis factor（TNF）-related apoptosis-inducing ligands （TRAIL）, a member of the tumor necrosis fac- tor superfamily , has been shown to predominantly kill cancer ceils, while preserving normal ceils. Failure to develop apoptosis in response to anticancer therapy may lead to drua resistance. Understanding the molecular e- vents that regulate apoptosis induced by anticancer therapy and how cancer cells evade apoptosis may provide new opportunities for drug development. Insights into the molecular mechanisms of cell death will guide to develop novel strategies targeting tumor cell resistance.
出处
《国际免疫学杂志》
CAS
北大核心
2010年第3期225-228,共4页
International Journal of Immunology
