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β-arrestins 在癌症侵袭和转移中的作用及其机制(综述)。

The role and mechanism of β‑arrestins in cancer invasion and metastasis (Review).

机构信息

Department of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.

出版信息

Int J Mol Med. 2018 Feb;41(2):631-639. doi: 10.3892/ijmm.2017.3288. Epub 2017 Nov 27.

DOI:10.3892/ijmm.2017.3288
PMID:29207104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5752234/
Abstract

β‑arrestins are a family of adaptor proteins that regulate the signaling and trafficking of various G protein‑coupled receptors (GPCRs). They consist of β‑arrestin1 and β‑arrestin2 and are considered to be scaffolding proteins. β‑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 β‑arrestins serve roles in various physiological and pathological processes and exhibit a similar function to GPCRs. β‑arrestins serve primary roles in cancer invasion and metastasis via various signaling pathways. The present review assessed the function and mechanism of β‑arrestins in cancer invasion and metastasis via multiple signaling pathways, including mitogen‑activated protein kinase/extracellular signal regulated kinase, Wnt/β‑catenin, nuclear factor‑κB and phosphoinositide‑3 kinase/Akt.

摘要

β-arrestins 是一类衔接蛋白家族,可调节各种 G 蛋白偶联受体 (GPCR) 的信号转导和转运。它们由 β-arrestin1 和 β-arrestin2 组成,被认为是支架蛋白。β-arrestins 调节细胞增殖,促进细胞侵袭和迁移,传递抗细胞凋亡的存活信号,并影响肿瘤的其他特征,包括肿瘤生长速度、血管生成、耐药性、侵袭和转移潜能。已经证实,β-arrestins 在各种生理和病理过程中发挥作用,并且与 GPCR 具有相似的功能。β-arrestins 通过多种信号通路在癌症侵袭和转移中发挥主要作用。本综述通过丝裂原活化蛋白激酶/细胞外信号调节激酶、Wnt/β-catenin、核因子-κB 和磷酸肌醇 3 激酶/Akt 等多种信号通路,评估了β-arrestins 在癌症侵袭和转移中的功能和机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/6087d64cb389/IJMM-41-02-0631-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/8f86b7a28fd0/IJMM-41-02-0631-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/59ee0add2bee/IJMM-41-02-0631-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/ad110cae4773/IJMM-41-02-0631-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/6087d64cb389/IJMM-41-02-0631-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/8f86b7a28fd0/IJMM-41-02-0631-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/59ee0add2bee/IJMM-41-02-0631-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/ad110cae4773/IJMM-41-02-0631-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/051a/5752234/6087d64cb389/IJMM-41-02-0631-g04.jpg

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