癌前生态位(PCN),由持续慢性炎症引起的纤维化和重塑的产物

4open Pub Date : 2019-01-01 DOI:10.1051/FOPEN/2018009
B. Brücher, I. Jamall
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引用次数: 10

摘要

成纤维细胞积极参与基质和细胞外基质的形成,这对细胞粘附、细胞间通讯和组织代谢至关重要。纤维化在癌变中的作用可以通过类比各种癌症的组织来检验。多种成分与信号和串扰相互作用中的字母编排尚不完全清楚,但现有证据表明迄今为止未被充分认识的纤维化在癌变中的作用。致病刺激引起的复杂信号和串扰引起持续的亚临床炎症,这反过来又导致不同细胞类型的级联,无处不在的蛋白质及其相应的酶,细胞因子的释放和多种信号通路促进纤维化的发生。有相当多的证据表明,人体试图解决这种改变的细胞外环境,导致体内平衡进一步破坏,癌前生态位的形成,这是描述癌变的六步过程的一部分。癌前生态位的形成和发展可以理解为:(1)致病性刺激,(2)慢性炎症,(3)细胞外基质、基质硬度和机械转导改变的纤维化。这就是为什么癌变不仅仅是一个遗传物质受损的异常细胞生长过程,而且PCN在整个过程中的作用揭示了癌变是如何在不需要体细胞突变的情况下发生的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation
Fibroblasts are actively involved in the creation of the stroma and the extracellular matrix which are important for cell adhesion, cell–cell communication, and tissue metabolism. The role of fibrosis in carcinogenesis can be examined by analogy to tissues of various cancers. The orchestration of letters in the interplay of manifold components with signaling and crosstalk is incompletely understood but available evidence suggests a hitherto underappreciated role for fibrosis in carcinogenesis. Complex signaling and crosstalk by pathogenic stimuli evoke persistent subclinical inflammation, which in turn, results in a cascade of different cell types, ubiquitous proteins and their corresponding enzymes, cytokine releases, and multiple signaling pathways promoting the onset of fibrosis. There is considerable evidence that the body's attempt to resolve such a modified extracellular environment leads to further disruption of homeostasis and the genesis of the precancerous niche as part of the six-step process that describes carcinogenesis. The precancerous niche is formed and can be understood to develop as a result of (1) pathogenic stimulus, (2) chronic inflammation, and (3) fibrosis with alterations of the extracellular matrix, stromal rigidity, and mechano-transduction. This is why carcinogenesis is not just a process of aberrant cell growth with damaged genetic material but the role of the PCN in its entirety reveals how carcinogenesis can occur without invoking the need for somatic mutations.
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