The role and mechanism of β-arrestins in cancer invasion and metastasis

被引:56
作者
Song, Qing [1 ,2 ,3 ]
Ji, Qing [1 ,2 ]
Li, Qi [1 ,2 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, 528 Zhangheng Rd, Shanghai 201203, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst Integrat Med, 528 Zhangheng Rd, Shanghai 201203, Peoples R China
[3] Suzhou Hosp Tradit Chinese Med, Dept Med Oncol, Suzhou 215009, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
beta-arrestins; mechanism; cancer; invasion; metastasis; EPITHELIAL-MESENCHYMAL TRANSITION; NF-KAPPA-B; CELL-PROLIFERATION; DOWN-REGULATION; TUMOR MICROENVIRONMENT; SIGNALING PATHWAY; RECEPTOR; PROMOTES; CATENIN; MIGRATION;
D O I
10.3892/ijmm.2017.3288
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
beta-arrestins are a family of adaptor proteins that regulate the signaling and trafficking of various G protein-coupled receptors (GPCRs). They consist of beta-arrestin1 and beta-arrestin2 and are considered to be scaffolding proteins. beta-arrestins regulate cell proliferation, promote cell invasion and migration, transmit anti-apoptotic survival signals and affect other characteristics of tumors, including tumor growth rate, angiogenesis, drug resistance, invasion and metastatic potential. It has been demonstrated that beta-arrestins serve roles in various physiological and pathological processes and exhibit a similar function to GPCRs. beta-arrestins serve primary roles in cancer invasion and metastasis via various signaling pathways. The present review assessed the function and mechanism of beta-arrestins in cancer invasion and metastasis via multiple signaling pathways, including mitogen-activated protein kinase/extracellular signal regulated kinase, Wnt/beta-catenin, nuclear factor-kappa B and phosphoinositide-3 kinase/Akt.
引用
收藏
页码:631 / 639
页数:9
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