Rbm17, also known as SPF45, is a splicing factor that plays a crucial role in pre-mRNA splicing. It is involved in the splicing of a subset of human short introns, where it can functionally substitute for U2AF on short introns with truncated polypyrimidine tracts [3,4,8]. Rbm17 also interacts with other spliceosomal factors like U2SURP and CHERP, reciprocally regulating their stability and influencing the splicing and gene expression of RNA-processing factors [9].

In cancer research, Rbm17 has been shown to have significant impacts. In acute myeloid leukemia (AML), its upregulation preferentially marks and sustains leukemic stem cells (LSCs), and its knockdown in primary AML cells leads to myeloid differentiation, impaired colony formation, and in vivo engraftment [1]. In non-small cell lung cancer (NSCLC) with low PD-L1 expression, Rbm17 expression is associated with a better objective response rate and progression-free survival in the ICI monotherapy group [2]. In hypopharyngeal cancer cells, downregulation of Rbm17 enhances cisplatin sensitivity and inhibits cell invasion [5]. In glioma, high Rbm17 expression is associated with poor prognosis, and its downregulation induces cell cycle arrest and apoptosis [6]. In colorectal cancer, Rbm17 enhances cell proliferation, reduces chemotherapy-induced apoptosis, and increases cancer stem cell properties through the AKT1-Rbm17-FOXM1-Sox2 axis [7]. In hepatocellular carcinoma (HCC), Rbm17 is overexpressed, and its knockdown reduces cell proliferation, arrests the cell cycle, and increases apoptosis [10].

In conclusion, Rbm17 is an important splicing factor involved in pre-mRNA splicing, especially for a subset of short introns. Model-based research, especially loss-of-function experiments in cancer cells, has revealed its oncogenic roles in multiple cancers, making it a potential therapeutic target in diseases such as AML, NSCLC, hypopharyngeal cancer, glioma, colorectal cancer, and HCC.