Abstract
The biogenesis of ribosomes is a finely regulated multistep process linked to cell proliferation and growth—processes which require a high rate of protein synthesis. One of the master regulators of ribosome biogenesis is Myc, a well-known proto-oncogene that has an important role in ribosomal function and in the regulation of protein synthesis. The relationship between Myc and the ribosomes was first highlighted in Drosophila, where Myc’s role in controlling Pol-I, II and III was evidenced by both microarrays data, and by the ability of Myc to control growth (mass), and cellular and animal size. Moreover, Myc can induce cell competition, a physiological mechanism through which cells with greater fitness grow better and thereby prevail over less competitive cells, which are actively eliminated by apoptosis. Myc-induced cell competition was shown to regulate both vertebrate development and tumor promotion; however, how these functions are linked to Myc’s control of ribosome biogenesis, protein synthesis and growth is not clear yet. In this review, we will discuss the major pathways that link Myc to ribosomal biogenesis, also in light of its function in cell competition, and how these mechanisms may reflect its role in favoring tumor promotion.
Highlights
Alterations in ribosome biogenesis due to mutations in genes encoding for ribosomal proteins is associated with the development of rare pathological diseases known as ribosomopathies, each of them characterized by specific defects in ribosome biogenesis and distinct clinical phenotypes
In this case a modest reduction in the expression of a single ribosomal protein gene was sufficient to reduce Myc ability to promote tumor onset [84]. Another stronger indication that increased ribosome biogenesis can be a direct cause of malignant transformation was provided by Devlin et al, who have demonstrated that synergistically targeting ribosome biogenesis and mRNA translation increased survival in Myc-driven lymphoma [137]
Many mutations in ribosomal proteins have been shown to cause a predisposition to cancer, including some linked to Myc activation
Summary
Ribosomes are the molecular machines responsible for decoding mRNAs into proteins. In eukaryotes, the ribosome is composed of the 40S and 60S subunits that associate to form the translationally active 80S ribosome. [10], In thetonucleolus, transcription of H/ACA-snoRNPs rDNA genes is mediated by RNA polymerase and other protein-processing factors responsible for the majority of rRNA modifications [11,12,13]. The small 40S ribosomal subunit post-transcriptionally modified to introduce a methyl group at the 2-O position of the ribose sugar contains one 18S rRNA and 32 ribosomal proteins (known as RPS), whereas the large 60S subunit is residues and pseudouridines. These modifications are mediated by the interaction with snoRNPs, composed of one of each 5S, 5.8S and 28S rRNA and 47 ribosomal proteins (known as RPL).
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