p21和p27在肿瘤发生机制中的作用与耐药性  

Role of p21 and p27 in carcinogenesis and drug resistance

作　　者：郑丽华[1] 赵亚恒[1] 刘运江[1] 

机构地区：[1]河北医科大学第四医院普外一科,石家庄050030

出　　处：《国际外科学杂志》2014年第7期494-498,共5页International Journal of Surgery

摘　　要：人类肿瘤的发生是由于细胞生长和死亡的不平衡导致的.控制这个平衡的关键是调节细胞周期的蛋白.目前发现的与密切调节细胞周期特定阶段效应分子包括细胞周期蛋白,细胞周期蛋白依赖性激酶（cyclin-dependent kinases CDKs）和CDK抑制因子.G1期检测点的CDK抑制因子-p21（CDKN1 A）和p27（CDKN1 B）影响许多恶性肿瘤的发生发展.越来越多的证据表明p21或p27功能的缺失可以促进耐药.而另外一些实验证明p21和p27能促进肿瘤的发生发展.在本文中,我们将讨论这两个CDK抑制因子的功能,在肿瘤发生机制以及在耐药性中的作用.Human cancers arise from an imbalance of cell growth and cell death.Critical factors that control the balance are those regulate the cell cycle.Several molecular effectors have been identified to be able to regulate specific phases of the cell cycle,including cyclins,cyclin-dependent kinases （CDKs） and CDK inhibitors.Notably,deficiency of two G1-checkpoint CDK inhibitors-p21 （CDKN1A） and p27 （CDKN1B）-has been implicated to be correlated with initiation or progression of many human malignancies or cancer cells drug-resistance.However,contradict reports also suggested that p21 and p27 could promote tumor progression.Here,we summarized the historic and recent studies on these two CDK inhibitors,including their identification as well as their roles in carcinogenesis and drug resistance.

关 键 词：周期素依赖激酶抑制剂p21 周期素依赖激酶抑制剂P27 抗药性 肿瘤 

分 类 号：R730.2[医药卫生—肿瘤]