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Pathol Res Pract. 2015 Aug;211(8):557-69. doi: 10.1016/j.prp.2015.05.010. Epub 2015 May 28.

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

Author information

1
Department of Pathology, School of Medicine, Zhejiang University, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Hangzhou 310058, China.
2
Department of Pathology, School of Medicine, Zhejiang University, Hangzhou 310058, China; Zhejiang Normal University-Jinhua People's Hospital Joint Center for Biomedical Research, Jinhua 321004, China.
3
Department of Pathology, School of Medicine, Zhejiang University, Hangzhou 310058, China; Key Laboratory of Disease Proteomics of Zhejiang Province, Hangzhou 310058, China. Electronic address: lmp@zju.edu.cn.

Abstract

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.

KEYWORDS:

Colorectal cancer; Epithelial–mesenchymal transition; Malignant phenotypes; Metastasis; Molecular related network

PMID:
26092594
DOI:
10.1016/j.prp.2015.05.010
[Indexed for MEDLINE]

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