Activation of Notch-1 signaling maintains the neoplastic phenotype in human Ras-transformed cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-08-19

AUTHORS

Sanne Weijzen, Paola Rizzo, Mike Braid, Radhika Vaishnav, Suzanne M. Jonkheer, Andrei Zlobin, Barbara A. Osborne, Sridevi Gottipati, Jon C. Aster, William C. Hahn, Michael Rudolf, Kalliopi Siziopikou, W. Martin Kast, Lucio Miele

ABSTRACT

Truncated Notch receptors have transforming activity in vitro and in vivo. However, the role of wild-type Notch signaling in neoplastic transformation remains unclear. Ras signaling is deregulated in a large fraction of human malignancies and is a major target for the development of novel cancer treatments. We show that oncogenic Ras activates Notch signaling and that wild-type Notch-1 is necessary to maintain the neoplastic phenotype in Ras-transformed human cells in vitro and in vivo. Oncogenic Ras increases levels and activity of the intracellular form of wild-type Notch-1, and upregulates Notch ligand Delta-1 and also presenilin-1, a protein involved in Notch processing, through a p38-mediated pathway. These observations place Notch signaling among key downstream effectors of oncogenic Ras and suggest that it might be a novel therapeutic target. More... »

PAGES

979-986

References to SciGraph publications

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  • Journal

    TITLE

    Nature Medicine

    ISSUE

    9

    VOLUME

    8

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm754

    DOI

    http://dx.doi.org/10.1038/nm754

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1013090465

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12185362


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