细胞外基质:休眠到转移生长转变过程中的守门员。

Extracellular matrix: a gatekeeper in the transition from dormancy to metastatic growth.

机构信息

Department of Biology, Faculty of Sciences, Haifa University, Haifa, Israel.

出版信息

Eur J Cancer. 2010 May;46(7):1181-8. doi: 10.1016/j.ejca.2010.02.027. Epub 2010 Mar 19.

Abstract

Metastases can develop after apparently successful treatment of a primary tumour, sometimes following a period of tumour dormancy that can last for years. However, factors that regulate metastatic tumour dormancy remain poorly understood. Here we review the potential contribution of interactions between tumour cells and the microenvironment in metastatic sites, in regulating tumour dormancy vs. metastatic growth. We focus particularly on the potential role of the extracellular matrix (ECM) in regulating maintenance and release from dormancy. Tumour cells that fail to properly adhere to the ECM may enter a state of dormancy. The molecular and physical composition of the ECM can be affected by tumour cells themselves, as well as multiple stromal cell types. The roles of integrins, fibronectin, and collagen are discussed, as are factors that can change the ECM. A better understanding of the molecular details of the crosstalk between tumour cells and the ECM in secondary sites, and how these regulate the dormant state, may lead to improved therapeutic strategies to induce or maintain disseminated tumour cells in a dormant state, or alternatively to successfully eradicate dormant cells.

摘要

转移瘤可在原发性肿瘤的治疗明显成功后发生,有时在肿瘤休眠期后发生,该休眠期可持续数年。然而,调节转移性肿瘤休眠的因素仍知之甚少。本文综述了肿瘤细胞与转移部位微环境之间相互作用在调节肿瘤休眠与转移生长中的潜在作用。我们特别关注细胞外基质(ECM)在调节维持和休眠释放中的潜在作用。未能正确黏附于 ECM 的肿瘤细胞可能进入休眠状态。肿瘤细胞本身以及多种基质细胞类型均可影响 ECM 的分子和物理组成。本文讨论了整合素、纤连蛋白和胶原的作用,以及可改变 ECM 的因素。深入了解肿瘤细胞与次级部位 ECM 之间相互作用的分子细节,以及这些相互作用如何调节休眠状态,可能会促使人们制定出改善的治疗策略,诱导或维持播散的肿瘤细胞处于休眠状态,或者成功消灭休眠细胞。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索