Burkitt's lymphoma-associated c-Myc mutations converge on a dramatically altered target gene response and implicate Nol5a/Nop56 in oncogenesis.
Burkitt's lymphoma-associated c-Myc mutations converge on a dramatically altered target gene response and implicate Nol5a/Nop56 in oncogenesis.
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伯基特淋巴瘤（BL）在Myc的保守结构域Myc盒I中获得一致的点突变。我们报告说，BL相关的Myc突变体的转化活性增强，可以从磷酸化的损失和蛋白质稳定性增加解偶联。此外，两种不同的BL相关的Myc突变诱导类似的基因表达谱独立于T58磷酸化，这些谱是显着不同的MycWT。rRNA甲基化所需的Nol 5a/Nop 56被鉴定为BL相关Myc突变体过度激活的基因。我们表明，Nol 5a是Myc诱导的细胞转化所必需的，增强了MycWT诱导的细胞转化，并增加了MycWT诱导的肿瘤的大小。因此，Nol 5a扩展了Myc诱导的核仁靶基因调节之间的联系，所述核仁靶基因是细胞转化和肿瘤生长的限速基因。
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 rRNA 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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