Notch3-mediated regulation of MKP-1 levels promotes survival of T acute lymphoblastic leukemia cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-04

AUTHORS

M Masiero, S Minuzzo, I Pusceddu, L Moserle, L Persano, V Agnusdei, V Tosello, G Basso, A Amadori, S Indraccolo

ABSTRACT

Activation of the Notch pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) because of mutations in Notch1 or Fbw7 and is involved in the regulation of cell proliferation and survival. Deregulated Notch3 signalling has also been shown to promote leukemogenesis in transgenic mice, but the targets of Notch3 in human T-ALL cells remain poorly characterized. Here, we show that Notch3 controls levels of mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1). In a model of T-ALL cell dormancy, both Notch3 activation and MKP-1 expression were upregulated in aggressive compared with dormant tumors, and this inversely correlated with the levels of phosphorylated p38 and extracellular signal-regulated kinase1/2 (ERK1/2) MAPKs, two canonical MKP-1 targets. We demonstrate that MKP-1 protein levels are regulated by Notch3 in T-ALL cell lines because its silencing by RNA interference or treatment with γ-secretase inhibitors induced strong MKP-1 reduction whereas activation of Notch3 signalling had the opposite effect. Furthermore, MKP-1 has an important role in T-ALL cell survival because its attenuation by short hairpin RNA significantly increased cell death under stress conditions. This protective function has a key role in vivo, as MKP-1-deficient cells showed impaired tumorigenicity. These results elucidate a novel mechanism downstream of Notch3 that controls the survival of T-ALL cells. More... »

PAGES

588

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/leu.2010.323

DOI

http://dx.doi.org/10.1038/leu.2010.323

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007152732

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21263446


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