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整合素相互作用促成信号传导的复杂性和不可预测的癌细胞命运。

Integrin Crosstalk Contributes to the Complexity of Signalling and Unpredictable Cancer Cell Fates.

作者信息

Samaržija Ivana, Dekanić Ana, Humphries Jonathan D, Paradžik Mladen, Stojanović Nikolina, Humphries Martin J, Ambriović-Ristov Andreja

机构信息

Laboratory for Cell Biology and Signalling, Division of Molecular Biology, Ruđer Bošković Institute, 10000 Zagreb, Croatia.

Laboratory for Protein Dynamics, Division of Molecular Medicine, Ruđer Bošković Institute, 10000 Zagreb, Croatia.

出版信息

Cancers (Basel). 2020 Jul 15;12(7):1910. doi: 10.3390/cancers12071910.

DOI:10.3390/cancers12071910
PMID:32679769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7409212/
Abstract

Integrins are heterodimeric cell surface receptors composed of α and β subunits that control adhesion, proliferation and gene expression. The integrin heterodimer binding to ligand reorganises the cytoskeletal networks and triggers multiple signalling pathways that can cause changes in cell cycle, proliferation, differentiation, survival and motility. In addition, integrins have been identified as targets for many different diseases, including cancer. Integrin crosstalk is a mechanism by which a change in the expression of a certain integrin subunit or the activation of an integrin heterodimer may interfere with the expression and/or activation of other integrin subunit(s) in the very same cell. Here, we review the evidence for integrin crosstalk in a range of cellular systems, with a particular emphasis on cancer. We describe the molecular mechanisms of integrin crosstalk, the effects of cell fate determination, and the contribution of crosstalk to therapeutic outcomes. Our intention is to raise awareness of integrin crosstalk events such that the contribution of the phenomenon can be taken into account when researching the biological or pathophysiological roles of integrins.

摘要

整合素是由α和β亚基组成的异二聚体细胞表面受体,可控制细胞黏附、增殖和基因表达。整合素异二聚体与配体结合会重组细胞骨架网络,并触发多种信号通路,这些信号通路可导致细胞周期、增殖、分化、存活和运动性的变化。此外,整合素已被确定为包括癌症在内的许多不同疾病的靶点。整合素串扰是一种机制,通过这种机制,特定整合素亚基表达的变化或整合素异二聚体的激活可能会干扰同一细胞中其他整合素亚基的表达和/或激活。在这里,我们综述了一系列细胞系统中整合素串扰的证据,特别强调癌症。我们描述了整合素串扰的分子机制、细胞命运决定的影响以及串扰对治疗结果的贡献。我们的目的是提高对整合素串扰事件的认识,以便在研究整合素的生物学或病理生理作用时能够考虑到这一现象的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/386397f7c0f7/cancers-12-01910-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/58e8380b6567/cancers-12-01910-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/2b025c733c57/cancers-12-01910-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/6dd5173f5f22/cancers-12-01910-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/386397f7c0f7/cancers-12-01910-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/58e8380b6567/cancers-12-01910-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/2b025c733c57/cancers-12-01910-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/6dd5173f5f22/cancers-12-01910-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6519/7409212/386397f7c0f7/cancers-12-01910-g004.jpg

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