Rbm15, an RNA-binding protein, is a crucial "writer" of the m6A methyltransferase complex. N6-methyladenosine (m6A) is a prevalent and conserved internal cotranscriptional modification in eukaryotic RNAs. Rbm15 regulates multiple signal pathways such as Notch and Wnt, playing important roles in cell growth, apoptosis, especially in blood cells [3].

In laryngeal squamous cell carcinoma (LSCC), knockdown of Rbm15 reduced cell proliferation, invasion, migration, and promoted apoptosis both in vitro and in vivo, as it regulates TMBIM6 stability through an IGF2BP3-dependent mechanism [1]. In lung adenocarcinoma, overexpression of Rbm15 increased m6A levels and promoted cell invasion, migration, and proliferation, while knockdown had opposite effects. Rbm15-mediated m6A modification inhibits RASSF8 protein levels to increase cell invasion and migration [2]. In triple-negative breast cancer, Rbm15 drives cell growth by stimulating serine and glycine metabolism [4]. In lung cancer, Rbm15 silencing promoted ferroptosis by regulating the TGF-β/Smad2 pathway, reducing cell viability, proliferation, invasion, and migration [5]. In lung adenocarcinoma, Rbm15 overexpression facilitated osimertinib resistance by enhancing m6A modification of SPOCK1 mRNA [6].

In conclusion, Rbm15 is significantly involved in the development and progression of multiple cancers, playing a key role in processes like cell proliferation, invasion, migration, apoptosis, and drug resistance. The study of Rbm15 through gene-knockout or knockdown models in these cancer-related disease areas has provided valuable insights into its functions, offering potential therapeutic targets for cancer treatment.