Journal
ONCOGENE
Volume 33, Issue 27, Pages 3519-3527Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2013.338
Keywords
Myc; lymphoma; mutations; Burkitt's; transcription
Funding
- National Cancer Institute [CA055248]
- National Institute of General Medical Sciences [T32GM008704]
- MRC [G0700240, MR/K024213/1] Funding Source: UKRI
- Medical Research Council [MR/K024213/1, G0700240] Funding Source: researchfish
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Burkitt's lymphomas (BLs) acquire consistent point mutations in a conserved domain of Myc, Myc Box I. We report that the enhanced transforming activity of BL-associated Myc mutants can be uncoupled from loss of phosphorylation and increased protein stability. Furthermore, two different BL-associated Myc mutations induced similar gene expression profiles independently of T58 phosphorylation, and these profiles are dramatically different from MycWT. Nol5a/Nop56, which is required for ribosomal RNA methylation, was identified as a gene hyperactivated by the BL-associated Myc mutants. We show that Nol5a is necessary for Myc-induced cell transformation, enhances MycWT-induced cell transformation and increases the size of MycWT-induced tumors. Thus, Nol5a expands the link between Myc-induced regulation of nucleolar target genes, which are rate limiting for cell transformation and tumor growth.
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