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细胞外基质在肿瘤发生和进展过程中作用的新见解。

New insights into the role of extracellular matrix during tumor onset and progression.

作者信息

Pupa Serenella M, Ménard Sylvie, Forti Stefania, Tagliabue Elda

机构信息

Molecular Targeting Unit, Department of Experimental Oncology, Istituto Nazionale Tumori, Milan, Italy.

出版信息

J Cell Physiol. 2002 Sep;192(3):259-67. doi: 10.1002/jcp.10142.

Abstract

Recently, a view of the tumor as a functional tissue interconnected with the microenvironment has recently been described. For many years, the stroma has been studied in the context of the malignant lesion, and only rarely has its role been considered before carcinogenic lesions appear. Recent studies have provided evidence that stromal cells and their products can cause the transformation of adjacent cells through transient signaling that leads to the disruption of homeostatic regulation, including control of tissue architecture, adhesion, cell death, and proliferation. It is now well established that tumor progression requires a continually evolving network of interactions between neoplastic cells and extracellular matrix. A relevant step of this process is the remodeling of microenvironment which surrounds tumors leading to the release of ECM-associated growth factors which can then stimulate tumor and/or endothelial cells. Finally, tumor cells reorganizing the extracellular matrix to facilitate communications and escape the homeostatic control exerted by the microenvironment modify response to cytotoxic treatments.

摘要

最近,肿瘤被描述为一种与微环境相互连接的功能性组织。多年来,人们一直在恶性病变的背景下研究基质,而在致癌性病变出现之前,其作用很少被考虑。最近的研究提供了证据,表明基质细胞及其产物可通过短暂信号传导导致相邻细胞发生转化,这种信号传导会破坏包括组织结构、黏附、细胞死亡和增殖控制在内的稳态调节。现在已经明确,肿瘤进展需要肿瘤细胞与细胞外基质之间不断演变的相互作用网络。这一过程的一个相关步骤是肿瘤周围微环境的重塑,导致与细胞外基质相关的生长因子释放,进而刺激肿瘤细胞和/或内皮细胞。最后,肿瘤细胞重组细胞外基质以促进通讯并逃避微环境施加的稳态控制,从而改变对细胞毒性治疗的反应。

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