摘要
胰岛素增强子结合蛋白-1(insulin gene enhancer binding protein-1,ISL1)是一种含两个LIM结构域和一个HD(homeodomain)结构域的转录因子,已被证明能调节多种信号通路和生物进程。在正常组织细胞中,ISL1通过与多个转录因子相互作用来精确调控靶基因表达从而促进细胞的分化、增殖等生物学过程。在肿瘤细胞中,ISL1通过影响细胞增殖和转移以及其他细胞过程最终在癌症的发生和发展中发挥作用。该文回顾ISL1参与的调控网络如何影响细胞增殖和肿瘤发生,细胞分化,细胞迁移、侵袭和转移,细胞凋亡。在不同的细胞中,ISL1的表达受不同的蛋白信号调控,并与不同的分子协同作用对细胞生物进程产生相应的影响,通过探究与ISL1功能相关的蛋白和信号通路,揭示正常组织发育和疾病的发生发展规律,为进一步机制研究提供理论基础,也可为新药开发、临床诊断提供理论依据。
ISL1(insulin gene enhancer binding protein-1),a transcription factor containing two LIM domains and one HD(homeodomain),has been proven to regulate a variety of signaling pathways and biological processes.In normal tissue cells,ISL1 can precisely regulate the expression of target genes by combining with multiple transcription factors to promote cell differentiation,proliferation and other biological processes.In tumor cells,ISL1 plays an important role in the occurrence and development of cancer by affecting cell proliferation and metastasis as well as other cellular processes.This article reviews how the regulatory network involved in ISL1 affects cell proliferation and tumorigenesis;cell differentiation;cell migration,invasion and metastasis;apoptosis.In different cells,the expression of ISL1 is regulated by different signal proteins and cooperates with different molecules,which has a corresponding impact on the cell biological process.By exploring the proteins and signal pathways related to the function of ISL1,it is possible to reveal the rules of tissue development and the occurrence and development of diseases,and to provide a theoretical basis for further mechanism research,as well as a theoretical basis for the development of new drugs and clinical diagnosis.
作者
倪小梅
马莉
石琼
NI Xiaomei;MALi;SHI Qing(Department of Clinical Laboratory,the Third Affiliated Hospital of Kunming Medical University,Kunming 650118,China)
出处
《中国细胞生物学学报》
CAS
CSCD
2021年第8期1658-1664,共7页
Chinese Journal of Cell Biology
基金
国家自然科学基金(批准号:81760426)资助的课题。
关键词
ISL1
细胞增殖
细胞分化
细胞凋亡
细胞转移
ISL1
cell proliferation
cell differentiation
cell apoptosis
cell metastasis