Rbms2, short for RNA binding motif single stranded interacting protein 2, belongs to the RBM family with conserved RNA binding motifs RNP1 and RNP2. It is an RNA binding protein (RBP) and plays a role in regulating the metabolism of target RNAs. RBPs are known to be involved in various cellular processes such as cancer cell proliferation, metastasis, and chemotherapeutic sensitivity [1,2].

In breast cancer, Rbms2 acts as a tumor suppressor. Overexpression of Rbms2 in breast cancer cells enhances sensitivity to doxorubicin and promotes apoptosis in the presence of doxorubicin, while its inhibition shows the opposite effect. This is achieved by Rbms2 positively regulating BMF expression, increasing BMF-induced expression of cleaved caspase 3, cleaved caspase 9, and poly (ADP-Ribose) polymerase (PARP) [1]. Additionally, Rbms2 inhibits breast cancer cell proliferation by stabilizing P21 mRNA post-transcriptionally. It directly binds to the AU-rich element of the 3'-UTR region of P21 mRNA, and the anti-proliferation activity induced by Rbms2 overexpression can be rescued by interfering with P21 expression [2].

In kidney renal clear cell carcinoma (ccRCC), Rbms2 also functions as a tumor suppressor. Overexpression of Rbms2 curtails ccRCC cell proliferation and migration, and it is negatively associated with adverse clinico-pathological features like advanced TNM stage, serving as a prognostic predictor [3].

In summary, Rbms2 functions as a tumor suppressor in breast cancer and ccRCC. In breast cancer, it affects chemosensitivity to doxorubicin and cell proliferation, while in ccRCC, it impacts cell proliferation, migration, and prognosis. Studies on Rbms2, especially through in vitro and in vivo models, help in understanding its role in cancer development and progression, potentially providing new therapeutic targets for drug-resistant cancers [1,2,3].