Involvement of partial EMT in cancer progression

被引:556
作者
Saitoh, Masao [1 ]
机构
[1] Univ Yamanashi, Interdisciplinary Grad Sch Med, Ctr Med Educ & Sci, Dept Biol Chem, 1110 Shimokato, Chuo, Yamanashi 4093898, Japan
关键词
cancer; differentiation; E-cadherin; EMT; invasion; EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA; CELL INVASION; TUMOR-CELLS; SNAIL; METASTASIS; RECEPTORS; PROTEINS; RAS; FIBROBLASTS;
D O I
10.1093/jb/mvy047
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The epithelial-mesenchymal transition (EMT) provides an outstanding example of cellular plasticity during embryonic development and cancer progression. During EMT in embryonic development, epithelial cells lose all vestiges of their epithelial origin and acquire a fully mesenchymal phenotype, known as complete EMT, which is typically characterized by a so-called cadherin switch. Conversely, during EMT in cancer progression, cancer cells that originate from epithelial cells exhibit both mesenchymal and epithelial characteristics, that is the hybrid E/M phenotype in a process known as partial EMT. Partial EMT in cancer cells is thought to enhance their invasive properties, generate circulating tumour cells and cancer stem cells, and promote resistance to anti-cancer drugs. These phenotypic changes are regulated by extracellular matrix components, exosomes and soluble factors, which regulate several transcription factors known as EMT transcription factors. In this review, I summarize our current understanding of the EMT program during cancer progression.
引用
收藏
页码:257 / 264
页数:8
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