Deadly crosstalk: Notch signaling at the intersection of EMT and cancer stem cells

被引：293

作者：

Espinoza, Ingrid ^{[1
,2
]}

Miele, Lucio ^{[1
,3
]}

机构：

[1] Univ Mississippi, Inst Canc, Med Ctr, Jackson, MS 39216 USA

[2] Univ Mississippi, Dept Biochem, Med Ctr, Jackson, MS 39216 USA

[3] Univ Mississippi, Dept Pharmacol & Toxicol, Med Ctr, Jackson, MS 39216 USA

来源：

CANCER LETTERS | 2013年 / 341卷 / 01期

关键词：

Notch signaling; EMT; EndMT; Cancer stem cells; Notch inhibitors; EPITHELIAL-MESENCHYMAL TRANSITION; BREAST-CANCER; TARGET; CHEMORESISTANCE; METASTASIS; ACTIVATION; EXPRESSION; PHENOTYPE; CLEAVAGE; RECEPTOR;

D O I：

10.1016/j.canlet.2013.08.027

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Notch signaling is an evolutionarily conserved pathway involved in cell fate control during development, stem cell self-renewal and postnatal tissue differentiation. Roles for Notch in carcinogenesis, in the biology of cancer stem cells, tumor angiogenesis and epithelial-to-mesenchymal transition (EMT) have been reported. This mini-review describes the role of Notch signaling deregulation in EMT and tumor aggressiveness. We describe how accumulated evidence suggests that Notch inhibition is an attractive strategy for the treatment of several cancers, at least in part because of its potential to reverse or prevent EMT. Published by Elsevier Ireland Ltd.

引用

页码：41 / 45

页数：5

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