Rbm22-KO Mouse

Rbm22, encoding an RNA-Binding Protein and belonging to the RNA-Binding Motif (RBM) family, has a structure suggesting a fusion of two yeast genes. It is mainly involved in pre-mRNA splicing, maintaining the conformation of the spliceosome's catalytic core and bridging it with other components. Rbm22 also participates in gene regulation by binding DNA as a transcription factor [1].

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 cell-cycle regulators [2]. In non-small cell lung cancer, RBM22 is underexpressed, and increasing its expression reduces tumorigenesis by stabilizing LATS1 mRNA [3]. In glioblastomas, dysregulation of RBM22 is observed, and its silencing decreases aggressiveness parameters in vitro and induces apoptosis [4]. In myeloid cells, RBM22 depletion delays cell-cycle progression and increases ploidy, and is partially responsible for the cytopenia phenotype in myelodysplastic syndromes with del(5q) [5].

In conclusion, Rbm22 plays essential roles in pre-mRNA splicing and gene regulation. Research on Rbm22 in various cancer models, such as prostate, lung, and glioblastoma cancers, as well as in myeloid cell-related diseases, has revealed its potential as a therapeutic target. Understanding Rbm22's functions contributes to our knowledge of disease mechanisms and may offer new strategies for treatment.

References:

1. Soubise, Benoît, Jiang, Yan, Douet-Guilbert, Nathalie, Troadec, Marie-Bérengère. 2022. RBM22, a Key Player of Pre-mRNA Splicing and Gene Expression Regulation, Is Altered in Cancer. In Cancers, 14, . doi:10.3390/cancers14030643. https://pubmed.ncbi.nlm.nih.gov/35158909/

2. Jiménez-Vacas, Juan M, Montero-Hidalgo, Antonio J, Gómez-Gómez, Enrique, Gahete, Manuel D, Luque, Raul M. 2022. Tumor suppressor role of RBM22 in prostate cancer acting as a dual-factor regulating alternative splicing and transcription of key oncogenic genes. In Translational research : the journal of laboratory and clinical medicine, 253, 68-79. doi:10.1016/j.trsl.2022.08.016. https://pubmed.ncbi.nlm.nih.gov/36089245/

3. Hou, Min, Huang, Qingmei, Chen, Shan, Lei, Jing, Zhang, Yakun. 2024. RNA binding protein RBM22 suppresses non-small cell lung cancer tumorigenesis by stabilizing LATS1 mRNA. In Journal of molecular histology, 56, 15. doi:10.1007/s10735-024-10285-3. https://pubmed.ncbi.nlm.nih.gov/39612045/

4. Fuentes-Fayos, Antonio C, Vázquez-Borrego, Mari C, Jiménez-Vacas, Juan M, Castaño, Justo P, Luque, Raúl M. . Splicing machinery dysregulation drives glioblastoma development/aggressiveness: oncogenic role of SRSF3. In Brain : a journal of neurology, 143, 3273-3293. doi:10.1093/brain/awaa273. https://pubmed.ncbi.nlm.nih.gov/33141183/

5. Le Hir-Reynaud, Eloïse, Soubise, Benoît, Mendoza, Abrahan Molina, Douet-Guilbert, Nathalie, Troadec, Marie-Bérengère. 2025. RBM22-depletion delays progression through all steps of cell cycle and increases ploidy in myeloid cells. In Biochimica et biophysica acta. Molecular cell research, 1872, 119965. doi:10.1016/j.bbamcr.2025.119965. https://pubmed.ncbi.nlm.nih.gov/40268057/