National Cancer Institute, Division of Cancer Treatment and Diagnosis, Cancer Therapy Evaluation Program, Investigational Drug Branch, Rockville, Maryland 20852, USA.
Breast Cancer Res. 2011 Jun 10;13(3):211. doi: 10.1186/bcr2876.
Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.
诱导癌症干细胞（CSC）中的上皮-间充质转化（EMT）可能是胚胎途径信号的结果。 Hedgehog（Hh）、Wnt、Notch 或转化生长因子-β 的激活导致一组转录因子的上调，这些转录因子驱动 EMT。这一过程导致黏附性差、非移动、上皮样肿瘤细胞转化为具有移动性、侵袭性表型的细胞。CSC 和 EMT 过程目前正在研究它们在乳腺癌中驱动转移性肿瘤形成中的作用。它们都与刺激 CSC 自我更新特性和 EMT 诱导转录因子的胚胎信号通路密切相关。了解这些机制和胚胎信号通路可能为开发治疗药物提供新的机会，以帮助预防乳腺癌的转移。在这篇综述中，我们研究了胚胎信号通路、CSC 和影响 EMT 的因素。
