肿瘤细胞通过激活MAPK途径的耐药相关机制  

Drug-Resistant Mechanism of Tumor Cells by Activating MAPK Path-way

作　　者：张如意[1] 郭雨声 罗瑛[1] 贾舒婷[1] 

机构地区：[1]昆明理工大学医学院衰老与肿瘤分子遗传学实验室,昆明市650500

出　　处：《医学分子生物学杂志》2016年第4期238-243,共6页Journal of Medical Molecular Biology

基　　金：国家自然科学基金（No.81460457）

摘　　要：丝裂原活化蛋白激酶（ mitogen－activated protein kinase， MAPK）信号途径是调节细胞增殖、生长、分化、凋亡、黏附和迁移的细胞内信号转导的重要通路。近年来的研究发现MAPK信号转导途径不仅与肿瘤的发生发展有关，激活的MAPK可能与肿瘤细胞耐药相关。文章围绕MAPK3条主要通路： ERK1／2、JNK、 p38从影响细胞药物外排，凋亡通路的异常，以及DNA损伤修复能力增强等方面阐述了MAPK调控肿瘤细胞的耐药机制。对于肿瘤细胞通过激活MAPK信号转导途径调控耐药发生发展机制的了解，将对临床上肿瘤靶向治疗药物的选择起到理论指导作用。Mitogen-activated protein kinases （ MAPK ） signaling pathways regulate multiple critical cellular functions including proliferation, growth, differentiation, apoptosis, adhesion and migration.In recent years, it was found that MAPK signal transduction pathway is associated with not only the development and progression of cancer but also drug resistance to promote tumorigene-sis, migration and other biological phenomena.Taking MAPK three pathways ERK1/2, JNK, p38 as the clue, this study summarized the mainly three resistance mechanisms of tumor cells：drug ef-flux, abnormal apoptosis and enhanced DNA damage repair ability, in an attempt to understand the drug-resistant mechanism of tumor cells by activating MAPK pathway.

关 键 词：MAPK途径 耐药机制 肿瘤 

分 类 号：R73-3[医药卫生—肿瘤]