Genome-wide occupancy of CNBP and SMARCC2 in neuroblastoma cells.

Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through integrated proteomics and validating studies, we discovered that CNBP physically interacted with SMARCC2 in NB cells. To investigate the mechanisms underlying the functions of CNBP and SMARCC2, we employed the Illumina Novaseq 6000 as a discovery platform to analyze the genome-wide occupancy of CNBP and SMARCC2 on target genes in human IMR-32 cells, while the results were further analyzed with CNBP-regulated target genes. The results showed that CNBP repressed the enrichment of SMARCC2 on 124 target genes, especially those involved in ribosome biogenesis, including BYSL, NOP58, and RRP9. Furthermore, we validated the ChIP-seq results by real-time PCR with high identity. Overall, our results provided fundamental information about the genomic enrichment of CNBP and SMARCC2 in human NB cells, and these findings will help us understand the pathogenesis of NB. Examination of genome-wide occupancy of two different transcriptional regulators in neuroblastoma cells.