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Journal Article
Notch as a tumour suppressor
2017
Overview
Key Points
Notch signalling can be either oncogenic or tumour suppressive depending on the tissue and/or cellular context.
Notch signalling is tumour suppressive for various solid tumours, including squamous cell carcinoma in several epithelial tissues, subtypes of brain cancer, liver cancer and small-cell lung cancer.
Loss of Notch signalling can result in perturbed regulation of cell fate decisions in stem and progenitor cells, resulting in tumour development.
Loss of Notch signalling can also lead to stromal remodelling and the generation of a pro-tumorigenic microenvironment that promotes carcinogenesis.
In this Review, Nowell and Radtke outline the accumulating evidence that Notch functions as a tumour suppressor in a range of cancers, and present potential mechanisms by which loss of Notch signalling could promote tumorigenesis.
The Notch signalling cascade is an evolutionarily conserved pathway that has a crucial role in regulating development and homeostasis in various tissues. The cellular processes and events that it controls are diverse, and continued investigation over recent decades has revealed how the role of Notch signalling is multifaceted and highly context dependent. Consistent with the far-reaching impact that Notch has on development and homeostasis, aberrant activity of the pathway is also linked to the initiation and progression of several malignancies, and Notch can in fact be either oncogenic or tumour suppressive depending on the tissue and cellular context. The Notch pathway therefore represents an important target for therapeutic agents designed to treat many types of cancer. In this Review, we focus on the latest developments relating specifically to the tumour-suppressor activity of Notch signalling and discuss the potential mechanisms by which Notch can inhibit carcinogenesis in various tissues. Potential therapeutic strategies aimed at restoring or augmenting Notch-mediated tumour suppression will also be highlighted.
Publisher
Nature Publishing Group UK,Nature Publishing Group
