Rbm10, an RNA-binding protein, is crucial for regulating alternative splicing of primary transcripts [1,2,3,4,6]. It has been linked to various cellular processes and diseases. In the p53 pathway, Rbm10 is a regulator of the tumor suppressor p53, and its loss of function can lead to cancer-related phenotypes [2].

In an EGFR-driven lung adenocarcinoma (LUAD) mouse model, lung-specific ablation of Rbm10 promoted tumor development, similar to Trp53 ablation, leading to overlapping gene expression changes enriched in cancer-related pathways. Rbm10 loss also induced key RNA splicing changes in both mice and LUAD patients [5]. In thyroid cancers, Rbm10 loss-of-function mutations are enriched in those with distant metastases. Rbm10 loss generates exon inclusion in transcripts regulating ECM-cytoskeletal interactions, leading to RAC1 activation and metastatic competency in mouse HrasG12V/Rbm10KO thyrocytes [7].

In conclusion, Rbm10 plays a vital role in regulating alternative splicing and is involved in important cellular pathways like the p53 pathway. The use of gene knockout mouse models, such as in LUAD and thyroid cancer studies, has revealed its significance in tumorigenesis and metastasis. Understanding Rbm10's functions can potentially provide new therapeutic strategies for related diseases [2,5,7].