Rbm22, a gene encoding an RNA-Binding Protein (RBP) and belonging to the RNA-Binding Motif (RBM) family, plays crucial roles in pre-mRNA splicing and gene expression regulation [1]. Structurally, it has a Zinc Finger like and a Zinc Finger domain, an RNA-Recognition Motif (RRM), and a Proline-Rich domain, suggesting an evolutionary fusion of two yeast genes. It is essential for maintaining the conformation of the spliceosome's catalytic core and acts as a bridge within the spliceosome. Rbm22 is also involved in gene regulation, being able to bind DNA and act as a transcription factor [1].

In zebrafish, knockdown of Rbm22 leads to a truncated axis and developmental arrest of the head and tail, indicating its importance in early embryogenesis [4]. In myeloid cells, Rbm22-depletion delays progression through all steps of the cell cycle and increases ploidy, and is partially responsible for the cytopenia phenotype in myelodysplastic syndromes with a partial deletion of chromosome 5 [5]. In prostate cancer, Rbm22 levels are down-regulated, and its overexpression decreases cancer aggressiveness by dysregulating the splicing of numerous genes and down-regulating critical upstream regulators of the cell-cycle [2]. In non-small cell lung cancer, Rbm22 suppresses tumorigenesis by stabilizing LATS1 mRNA [3].

In conclusion, Rbm22 is essential for pre-mRNA splicing, gene expression regulation, and normal development. Its dysregulation is associated with various diseases, especially cancers. Studies using model organisms like zebrafish and in cell-based functional studies in cancer cell lines have provided insights into its role in biological processes and disease conditions, highlighting its potential as a therapeutic target in cancer [1,2,3,4,5].