SMN1 orchestrates the global transcriptome profile associated with neuropathic pain development in SHSY5Y cells

Survival of motor neuron 1 (SMN1) acts as an RNA-binding protein, exerts multiple biological effects, participates in the production of small ribonucleoproteins (snRNPs), and regulates RNA metabolism through post-transcriptional regulation. Previous studies have reported that SMN1 mediates neuronal death through the classical apoptotic pathway; however, the mechanism by which it regulates neuropathic pain (NP) remains unknown. In this study, we used transcriptome sequencing, observed that SMN1 overexpression significantly impacted gene expression, and obtained functional clusters of differentially expressed genes (DEGs) highly enriched in NP-related terms. These genes were mainly enriched in biological pathways related to cell adhesion, inflammatory response, and signal transduction. In addition, the overexpression of SMN1 also regulated the alternative splicing (AS) of genes related to biological pathways such as DNA damage stimulation and DNA repair. Our study showed that SMN1 might be involved in the occurrence and development of NP by regulating the transcriptional and AS levels of related genes. Overall design: We constructed a smn1 overexpression model in SHSY5Y cell line, coupled with RNA-seq sequences, to comprehensively reveal the biological function of SMN1 in SHSY5Y cell and analyze the alterations of transcriptional profiles upon SMN1 overexpression.