Abstract
Protein arginine methylation is a common post-translational modification involved in numerous cellular processes including transcription, DNA repair, mRNA splicing and signal transduction. Currently, there are nine known members of the protein arginine methyltransferase (PRMT) family, but only one arginine demethylase has been identified, namely the Jumonji domain-containing 6 (JMJD6). Although its demethylase activity was initially challenged, its dual activity as an arginine demethylase and a lysine hydroxylase is now recognized. Interestingly, a growing number of substrates for arginine methylation and demethylation play key roles in tumorigenesis. Though alterations in the sequence of these enzymes have not been identified in cancer, their overexpression is associated with various cancers, suggesting that they could constitute targets for therapeutic strategies. In this review, we present the recent knowledge of the involvement of PRMTs and JMJD6 in tumorigenesis.
Highlights
Protein methylation was first described in early 1960s, with the discovery of ε-N-methyl-lysine in the flagellar protein of Salmonella typhimurium [1]
The altered expression and/or enzymatic activity of the protein arginine methyltransferase (PRMT) and arginine demethylase are involved in breast tumorigenesis
PRMTs are very often overexpressed in tumors, implying that knock-out experiments cannot be used to decipher their molecular impact on cancer development
Summary
Protein methylation was first described in early 1960s, with the discovery of ε-N-methyl-lysine in the flagellar protein of Salmonella typhimurium [1]. Because of the involvement of its tumor suppressor activity in cell cycle transcription, DNA damage response and chromatin remodeling, a dysregulation in BRCA1 following aberrant methylation could result in genomic instability. This pathway is activated in aggressive breast tumors, and the high level of expression of this complex is an independent marker of poor prognosis, associated with reduced disease-free survival, supporting the idea that ERα hypermethylation could trigger abnormal cell proliferation [63].
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