The ribosomal RPL10 R98S mutation drives IRES-dependent BCL-2 translation in T-ALL View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-02

AUTHORS

Kim R. Kampen, Sergey O. Sulima, Benno Verbelen, Tiziana Girardi, Stijn Vereecke, Gianmarco Rinaldi, Jelle Verbeeck, Joyce Op de Beeck, Anne Uyttebroeck, Jules P. P. Meijerink, Anthony V. Moorman, Christine J. Harrison, Pieter Spincemaille, Jan Cools, David Cassiman, Sarah-Maria Fendt, Pieter Vermeersch, Kim De Keersmaecker

ABSTRACT

The R98S mutation in ribosomal protein L10 (RPL10 R98S) affects 8% of pediatric T-cell acute lymphoblastic leukemia (T-ALL) cases, and was previously described to impair cellular proliferation. The current study reveals that RPL10 R98S cells accumulate reactive oxygen species which promotes mitochondrial dysfunction and reduced ATP levels, causing the proliferation defect. RPL10 R98S mutant leukemia cells can survive high oxidative stress levels via a specific increase of IRES-mediated translation of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2), mediating BCL-2 protein overexpression. RPL10 R98S selective sensitivity to the clinically available Bcl-2 inhibitor Venetoclax (ABT-199) was supported by suppression of splenomegaly and the absence of human leukemia cells in the blood of T-ALL xenografted mice. These results shed new light on the oncogenic function of ribosomal mutations in cancer, provide a novel mechanism for BCL-2 upregulation in leukemia, and highlight BCL-2 inhibition as a novel therapeutic opportunity in RPL10 R98S defective T-ALL. More... »

PAGES

319-332

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41375-018-0176-z

DOI

http://dx.doi.org/10.1038/s41375-018-0176-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105014437

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29930300


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