坏死性凋亡调控机制及其在肿瘤病理机制中的作用  

Regulation mechanism of necroptosis and its role in cancer pathogenesis

作　　者：李莉 刘力[1,2] 罗宁 程忠平 Li Li;Liu Li;Luo Ning;Cheng Zhongping(Department of Obstetrics and Gynecology,Yangpu Hospital,Tongji University School of Medicine,Shanghai 200090,China;Institute of Gynecological Minimally Invasive Medicine,Tongji University School of Medicine,Shanghai 200090,China)

机构地区：[1]上海市同济大学附属杨浦医院妇产科,上海200090 [2]同济大学医学院妇科微创医学研究所,上海200090

出　　处：《现代肿瘤医学》2018年第22期3690-3695,共6页Journal of Modern Oncology

基　　金：上海市医学重点专科建设项目(编号:ZA2015A33)

摘　　要：坏死性凋亡是非caspase依赖的程序性细胞死亡形式,由受体相互作用蛋白激酶1/3(receptor interacting protein kinase 1/3,RIPK1/3)和混合连接激酶结构域样蛋白(mixed lineage kinase domain-like protein,MLKL)介导,具有与坏死相同的形态学特征。坏死性凋亡在肿瘤病理机制中具有双重作用,可以补偿性清除和杀灭凋亡耐受的肿瘤细胞,发挥抑制肿瘤效应;也可以通过激发肿瘤微环境炎症反应,促进肿瘤发生发展、侵袭转移。本文综述了坏死性凋亡的调控机制及其在肿瘤发生进展的生物学效应和病理学意义。Necroptosis is a caspase-independent form of programmed cell death mediated by RIPK1/RIPK3（ receptor-interacting protein kinase 1/3） and MLKL（ mixed-line kinase domain-like protein）,with the same morphological characteristics of necrosis. Necroptosis has dual roles in the pathogenesis of cancer. It can eliminate and kill the apoptosis-resistant cancer cells alternatively and play a role in anti-cancer effect. It can also stimulate the cancer microenvironment inflammatory responses promoting tumor development,invasion and metastasis. This review summarizes the research progress on mechanism of necroptosis and its biological effects and pathological significance in tumor progression.

关 键 词：凋亡 坏死性凋亡 肿瘤 RIPK3 MLKL 

分 类 号：R730.2[医药卫生—肿瘤]