The wound healing, chronic fibrosis, and cancer progression triad

被引：171
作者：
Rybinski, Brad [1 ]
Franco-Barraza, Janusz [1 ]
Cukierman, Edna [1 ]
机构：
[1] Fox Chase Canc Ctr Temple Hlth, Canc Biol Program, Philadelphia, PA USA
来源：
PHYSIOLOGICAL GENOMICS | 2014年 / 46卷 / 07期
关键词：
wound healing; regeneration; fibrosis; cancer; tumor stroma; myofibroblasts; tumor- or cancer-associated fibroblasts; desmoplasia; epithelial-to-mesenchymal transition; FIBROBLAST-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; PREOPERATIVE PLASMA-FIBRINOGEN; IDIOPATHIC PULMONARY-FIBROSIS; MODULATES MYOFIBROBLAST DIFFERENTIATION; PROTEASE-ACTIVATED RECEPTOR-1; EXPERIMENTAL HEPATIC-FIBROSIS; RENAL INTERSTITIAL FIBROSIS; TUMOR STROMA GENERATION; NATURAL-KILLER-CELLS;
D O I：
10.1152/physiolgenomics.00158.2013
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The wound healing, chronic fibrosis, and cancer progression triad. Physiol Genomics 46: 223-244,2014. First published February 11, 2014; doi:10.1152/physiolgenomics.00158.2013.- 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.
引用
收藏
页码：223 / 244
页数：22
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