Ye Xin, Weinberg Robert A
Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Ludwig Center for Molecular Oncology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Trends Cell Biol. 2015 Nov;25(11):675-686. doi: 10.1016/j.tcb.2015.07.012. Epub 2015 Oct 1.
The epithelial-mesenchymal transition (EMT) program has emerged as a central driver of tumor malignancy. Moreover, the recently uncovered link between passage through an EMT and acquisition of stem-like properties indicates that activation of the EMT programs serves as a major mechanism for generating cancer stem cells (CSCs); that is, a subpopulation of cancer cells that are responsible for initiating and propagating the disease. In this review, we summarize the evidence supporting the widespread involvement of the EMT program in tumor pathogenesis and attempt to rationalize the connection between the EMT program and acquisition of stem cell traits. We propose that epithelial-mesenchymal plasticity is likely controlled by multiple varients of the core EMT program, and foresee the need to resolve the various programs and the molecular mechanisms that underlie them.
上皮-间质转化(EMT)程序已成为肿瘤恶性发展的核心驱动因素。此外,最近发现的经历EMT与获得干细胞样特性之间的联系表明,EMT程序的激活是产生癌症干细胞(CSCs)的主要机制;也就是说,癌症干细胞是负责启动和传播疾病的癌细胞亚群。在本综述中,我们总结了支持EMT程序广泛参与肿瘤发病机制的证据,并试图阐明EMT程序与获得干细胞特性之间的联系。我们提出上皮-间质可塑性可能由核心EMT程序的多个变体控制,并预见需要解析各种程序及其潜在的分子机制。