Epithelial-mesenchymal transition in colorectal cancer metastasis: A system review

被引:317
作者
Cao, Hui [1 ,2 ]
Xu, Enping [1 ,2 ]
Liu, Hong [1 ,3 ]
Wan, Ledong [1 ,2 ]
lai, Maode [1 ,2 ]
机构
[1] Zhejiang Univ, Sch Med, Dept Pathol, Hangzhou 310058, Zhejiang, Peoples R China
[2] Key Lab Dis Prote Zhejiang Prov, Hangzhou 310058, Zhejiang, Peoples R China
[3] Zhejiang Normal Univ Jinhua Peoples Hosp Joint Ct, Jinhua 321004, Peoples R China
基金
中国国家自然科学基金;
关键词
Metastasis; Epithelial-mesenchymal transition; Molecular related network; Malignant phenotypes; Colorectal cancer; E-CADHERIN EXPRESSION; TRANSCRIPTION FACTOR SNAIL; BETA-CATENIN EXPRESSION; EPIDERMAL-GROWTH-FACTOR; NEGATIVE FEEDBACK LOOP; LYMPH-NODE METASTASIS; COLON-CARCINOMA CELLS; REPRESSES E-CADHERIN; VITAMIN-D-RECEPTOR; TGF-BETA;
D O I
10.1016/j.prp.2015.05.010
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Tumor metastasis is a multi-step process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. And metastasis is the major cause of death in the vast majority of cancer patients. However, the mechanisms underlying each step remain obscure. In the past decade, a developmental program epithelial-to-mesenchymal transition (EMT) has been increasingly recognized to play pivotal and intricate roles in promoting carcinoma invasion and metastasis. The EMT process is very complex and controlled by various families of transcriptional regulators through different signaling pathways. In this system review, we focus on the molecular network of the EMT program and its malignant phenotypes associated with metastasis in colorectal cancer (CRC), including cancer stem cells, tumor budding, circulating tumor cells and drug resistance. A better understanding of the molecular regulation of the dynamic EMT program during tumor metastasis will help to provide much-needed therapeutic interventions to target this program when treating metastatic CRC. (C) 2015 Elsevier GmbH. All rights reserved.
引用
收藏
页码:557 / 569
页数:13
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