A potential role for CCN2/CTGF in aggressive colorectal cancer

被引:32
作者
Ubink, Inge [1 ]
Verhaar, Elisha R. [2 ]
Kranenburg, Onno [1 ]
Goldschmeding, Roel [2 ,3 ]
机构
[1] Univ Med Ctr Utrecht, Ctr Canc, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands
[2] Univ Med Ctr Utrecht, Dept Pathol, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands
[3] Univ Med Ctr Utrecht, POB 85500, NL-3508 GA Utrecht, Netherlands
关键词
Colorectal cancer; Connective tissue growth factor; CCN2; Fibrosis; TISSUE GROWTH-FACTOR; STROMAL EXPRESSION; FACTOR CTGF/CCN2; TGF-BETA; PROGNOSIS; CTGF; METASTASIS; PREDICTOR; TUMORS; CELLS;
D O I
10.1007/s12079-016-0347-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
CCN2, also known as connective tissue growth factor (CTGF) is a transcriptional target of TGF-beta signaling. Unlike its original name ("CTGF") suggested, CCN2 is not an actual growth factor but a matricellular protein that plays an important role in fibrosis, inflammation and connective tissue remodeling in a variety of diseases, including cancer. In pancreatic ductal adenocarcinoma, CCN2 signaling induces stromal infiltration and facilitates a strong tumor-stromal interaction. In many types of cancer, CCN2 overexpression has been associated with poor outcome. CMS4 (Consensus Molecular Subtype 4) is a recently identified aggressive colorectal cancer subtype, that is characterized by up-regulation of genes involved in epithelial-tomesenchymal transition, TGF-beta signaling, angiogenesis, complement activation, and extracellular matrix remodeling. In addition, a high influx of stromal fibroblasts contributes to the mesenchymal-like gene expression profile of this subtype. Furthermore, compared with the other three CMS groups, CMS4 tumors have the worst prognosis. Based on these observations, we postulated that CCN2 might contribute to colorectal cancer progression, especially in the CMS4 subtype. This review discusses the available literature on the role of CCN2 in colorectal cancer, with a focus on the 'fibrotic subtype' CMS4.
引用
收藏
页码:223 / 227
页数:5
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