Phosphorylation of MCT-1 by p44/42 MAPK is required for its stabilization in response to DNA damage View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-04

AUTHORS

S Nandi, L S Reinert, A Hachem, K Mazan-Mamczarz, P Hagner, H He, R B Gartenhaus

ABSTRACT

We discovered a novel oncogene in a T-cell lymphoma cell line, multiple copies in T-cell lymphoma-1 (MCT-1), that has been shown to decrease cell-doubling time, shorten the duration of G(1) transit time and/or G(1)-S transition, and transform NIH3T3 fibroblasts. We subsequently demonstrated that there were significantly increased levels of MCT-1 protein in a subset of primary diffuse large B-cell lymphomas. Levels of MCT-1 protein were shown to be increased after exposure to DNA damaging agents. This increase did not require new protein synthesis, suggesting that post-translational mechanisms were involved. Phosphorylation is one potential mechanism by which the activity of molecules involved in cell cycle/survival is rapidly modulated. The RAS/mitogen-activated/extracellular-regulated kinase (MEK)/extracellular signal-regulated kinases (ERK) pathway plays a prominent role in the regulation of cell growth and proliferation through phosphorylation-dependent regulation of several substrates. The MCT-1 protein is predicted to have numerous putative phosphorylation sites. Using a combination of genetic and pharmacological approaches, we established that phosphorylation of MCT-1 protein by p44/p42 mitogen-activated protein kinases is critical for stabilization of MCT-1 protein and for its ability to promote cell proliferation. Our data suggests that targeting the RAS/MEK/ERK signal transduction cascade may provide a potential therapeutic approach in lymphomas and related malignancies that exhibit high levels of MCT-1 protein. More... »

PAGES

1210030

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1210030

DOI

http://dx.doi.org/10.1038/sj.onc.1210030

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043860660

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17016429


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