DBF4依赖性激酶在肿瘤发展与治疗中的作用研究进展  

Progress in the role of DBF4-dependent kinase in tumor development and treatment

作　　者：陈柳艳 梁瑶瑶 陈津 Chen Liuyan;Liang Yaoyao;Chen Jin(Institute of Clinical Medicine,the Second Affiliated Hospital of Hainan Medical University,Haikou 570311,China)

机构地区：[1]海南医学院第二附属医院临床医学研究所,海口570311

出　　处：《中华细胞与干细胞杂志（电子版）》2024年第1期56-61,共6页Chinese Journal of Cell and Stem Cell（Electronic Edition）

基　　金：海南省自然科学基金(822MS179);海南省重点研发项目(ZDYF2022SHFZ133)。

摘　　要：DBF4依赖性激酶(DDK)是由DBF4与CDC7结合形成,可激活解螺旋酶,在细胞的复制中发挥重要作用。DBF4作为调节亚基,还可以通过与其他蛋白结合,直接或间接地激活细胞周期激酶,进一步调节细胞周期。研究发现,在许多肿瘤中,DBF4基因持续高表达,致使DDK激酶的活化增多,这可能是癌症发生的基础。靶向抑制DDK,有可能抑制肿瘤的生长。因此本文将从DDK的结构与调节功能、DDK在肿瘤发展中的作用以及DDK抑制剂在抗肿瘤中的作用研究进展做一综述,以期为开发靶向肿瘤细胞周期治疗方法提供理论依据。DBF4-dependent kinase(DDK)is formed by the binding of DBF4 and CDC7,and it could activate helicase.This activation plays a crucial role in cell replication.DBF4,as a regulatory subunit,also activates cell cycle kinases directly or indirectly by interacting with other proteins.This interaction further regulates the cell cycle process.It has been shown that the DBF4 gene is continuously overexpressed in many tumors.The overexpression of DBF4 leads to DDK kinase activation,which might be the underlying reason for cancer development.Targeted inhibition of DDK potentially inhibits tumor growth.Therefore,this article provides a comprehensive review on the structure and regulatory function of DDK,the role of DDK in tumor development,and the application of DDK inhibitors in tumor treatment,in order to provide a theoretical basis for the development of targeted tumor cell cycle therapy methods.

关 键 词：DBF4 DBF4依赖性激酶 CDC7 DDK抑制剂 

分 类 号：R730.5[医药卫生—肿瘤]