Howard Hughes Medical Institute and Department of Pathology, NYU School of Medicine, New York, NY 10016, USA; NYU Cancer Institute and Helen L. and Martin S. Kimmel Center for Stem Cell Biology, NYU School of Medicine, New York, NY 10016, USA.
Departments of Pediatrics and Genetics, Stanford University, Stanford, CA 94305, USA.
Cancer Cell. 2014 Mar 17;25(3):318-34. doi: 10.1016/j.ccr.2014.02.018.
Since Notch phenotypes in Drosophila melanogaster were first identified 100 years ago, Notch signaling has been extensively characterized as a regulator of cell-fate decisions in a variety of organisms and tissues. However, in the past 20 years, accumulating evidence has linked alterations in the Notch pathway to tumorigenesis. In this review, we discuss the protumorigenic and tumor-suppressive functions of Notch signaling, and dissect the molecular mechanisms that underlie these functions in hematopoietic cancers and solid tumors. Finally, we link these mechanisms and observations to possible therapeutic strategies targeting the Notch pathway in human cancers.
自 100 年前首次在果蝇中鉴定出 Notch 表型以来， Notch 信号已被广泛描述为各种生物体和组织中细胞命运决定的调节剂。然而，在过去的 20 年中，越来越多的证据表明 Notch 途径的改变与肿瘤发生有关。在这篇综述中，我们讨论了 Notch 信号的促肿瘤和抑肿瘤功能，并剖析了这些功能在造血系统癌症和实体瘤中所基于的分子机制。最后，我们将这些机制和观察结果与针对人类癌症 Notch 途径的可能治疗策略联系起来。
