Potential link between m(6)A modification and systemic lupus erythematosus

The field of m(6)A modification and epitranscriptomics has recently attracted much attention. More methods allowing for precise m(6)A site profiling and location are developed and crucial players of m(6)A modification machinery are increasingly identified. Although some challenges remain, m(6)A modification is found to modulate almost all aspects of RNA metabolism, such as splicing, stability, structure, translation, and export. Thus, m(6)A modification adds a new layer of post-transcriptional gene expression regulation, and it is implicated in T cell response to HIV infection, type I interferon production, and T cell differentiation and homeostasis. Moreover, evidence supporting its involvement in various human diseases including cancers is accumulating. Given the role of m(6)A modification in gene expression regulation and immune response, it invites the speculation that m(6)A modification may justify the pathogenesis of systemic lupus erythematosus (SLE) and take part in the initiation and progression of SLE. In this review, we introduce the widespread existence of m(6)A modification and briefly discuss components of m(6)A modification machinery in mammals. We mainly summarize the studies reporting the mechanisms of m(6)A modification in gene expression regulation through modulating pre-mRNA splicing, mRNA stability, RNA structure, translation, and pri-miRNA processing. Biological functions related to immune response of m(6)A modification and the implication of m(6)A modification in cancers are highlighted. In the end, we surmise the potential link between m(6)A modification and SLE.