创伤愈合、慢性纤维化和癌症进展三联征。
The wound healing, chronic fibrosis, and cancer progression triad.
机构信息
Cancer Biology Program, Fox Chase Cancer Center/Temple Health, Philadelphia, Pennsylvania.
出版信息
Physiol Genomics. 2014 Apr 1;46(7):223-44. doi: 10.1152/physiolgenomics.00158.2013. Epub 2014 Feb 11.
Abstract
For decades tumors have been recognized as "wounds that do not heal." Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.
摘要
几十年来，肿瘤一直被认为是“无法愈合的伤口”。除了肿瘤和受伤组织之间的共同之处外，伤口愈合过程也表现出与慢性纤维化相似的特征。在这篇综述中，我们提出了一种紧密的相互关系，它被认为是伤口愈合、慢性纤维化和癌症发展/进展（即 WHFC 三联征）之间细胞和微环境反应的共存。很明显，相同的细胞类型以及通过不同信号通路驱动伤口愈合（包括再生）的可溶性和基质成分，也会引发慢性纤维化和肿瘤进展。因此，在这里我们通过伤口愈合的视角来回顾纤维化和癌症之间的关系。
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