SMC1A recruits tumor-associated-fibroblasts (TAFs) and promotes colorectal cancer metastasis

被引:26
|
作者
Zhou, Pengyang [1 ]
Xiao, Nan [1 ]
Wang, Jian [1 ]
Wang, Zhanhuai [1 ]
Zheng, Shuchun [1 ]
Shan, Siyang [1 ]
Wang, Jianping [2 ]
Du, Jinlin [2 ]
Wang, Jianwei [1 ]
机构
[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Surg Oncol, Hangzhou 310009, Zhejiang, Peoples R China
[2] Zhejiang Univ, Jinhua Hosp, Dept Colorectal & Anal Surg, Hangzhou, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
SMC1A; Colorectal liver metastasis; Tumor-associated-fibroblasts; Tumorigenesis; Recruitment; GROWTH; SURVIVAL;
D O I
10.1016/j.canlet.2016.10.041
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tumor-associated-fibroblasts (TAFs) are the most important host cells in the stroma and take part in extracellular matrix construction and cancer colony development. During cancer colonization, seed cells from primary tumor can reconstruct the microenvironment by recruiting circulating cancer cells and TAFs to the metastasis site. Previous studies have established that SMC1A, a subunit of cohesin, is an important trigger signal for liver metastasis in colorectal cancer. We investigated the particular effects as well as the underlying mechanism of SMC1A on TAFs recruitment during liver metastasis of colorectal cancer. Here, We found that: first, the high expression of SMC1A in colorectal cancer cells promotes the invasiveness and the viability of these cells by recruiting circulating TAFs, facilitating early tumor construction and tumorigenesis; second, different expression levels of SMC1A influenced the reformation of fibroblasts, which assisted tumorigenesis, and third, expression of SMC1A stimulated the secretion of the inflammatory mediators of TNF-alpha and IL-1 beta, and up-regulated the transcriptional expression of MMP2 and VEGF-beta, both of which were involved in the tumor-related gene pathway. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:39 / 45
页数:7
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