Rbm15, an RNA-binding protein, is a "writer" of the m6A methyltransferase. m6A is the most abundant and variable modification in mammalian mRNA, playing crucial roles in regulating RNA metabolism, which in turn affects various biological processes such as cell growth, apoptosis, and differentiation. Rbm15 is involved in multiple signal pathways like Notch and Wnt [3].

Knockdown of Rbm15 in laryngeal squamous cell carcinoma (LSCC) reduced cell proliferation, invasion, migration, and promoted apoptosis both in vitro and in vivo. Rbm15-mediated m6A modification enhanced the stability of TMBIM6 mRNA through IGF2BP3-dependent manner, thus facilitating LSCC progression [1].

In lung adenocarcinoma, knockdown of Rbm15 decreased m6A levels, and inhibited cell invasion, migration, and proliferation. Rbm15-mediated m6A modification inhibited RASSF8 protein levels, promoting cell invasion and migration [2].

In lung cancer, Rbm15 silencing reduced cell viability, inhibited proliferation, invasion, and migration, and promoted ferroptosis by regulating the TGF-β/Smad2 pathway [4].

In triple-negative breast cancer, Rbm15 drives cell growth through the stimulation of serine and glycine metabolism [5].

In lung adenocarcinoma, Rbm15 is overexpressed, facilitating tumor cell proliferation, migration, and osimertinib resistance by enhancing m6A modification of SPOCK1 mRNA [6].

In conclusion, Rbm15 plays essential roles in the progression of multiple cancers including LSCC, lung adenocarcinoma, and triple-negative breast cancer, mainly through m6A-mediated regulation of downstream target genes. Gene-knockout or knockdown models in these cancer-related studies have revealed the significant impact of Rbm15 on cell proliferation, invasion, migration, apoptosis, and drug resistance, providing potential therapeutic targets for these diseases.