RNA–binding motif protein 24 (RBM24) acts as a multifunctional determinant of cell fate, proliferation, apoptosis, and differentiation during development by regulating premRNA splicing and mRNA stability. It is also implicated in carcinogenesis, but the functions of RBM24 in bladder cancer (BC) remain unclear. In the present study, we revealed that RBM24 was upregulated in BC tissues. Importantly, we found that a higher level of RBM24 was correlated with poor prognosis in BC patients. Overexpression of RBM24 promoted BC cell proliferation, while depletion of RBM24 inhibited BC cell proliferation in vivo and in vitro. Mechanistically, RBM24 positively regulated Runx1t1 expression in BC cells by binding to and enhancing Runx1t1 mRNA stability. Furthermore, Runx1t1 in turn promoted RBM24 expression by interacting with the transcription factor TCF4 and suppressing the transcription of miR-625-5p, which directly targets RBM24 and suppresses RBM24 expression. RBM24-regulated BC cell proliferation was moderated via the Runx1t1/TCF4/miR-625-5p feedback loop. These results indicate that the RBM24/Runx1t1/TCF4/miR-625-5p positive feedback loop participates in BC progression. Disruption of this pathway may be a potential therapeutic strategy for BC treatment.

RNA 结合基序蛋白 24 (RBM24) 通过调节前 mRNA 剪接和 mRNA 稳定性，在发育过程中充当细胞命运、增殖、凋亡和分化的多功能决定因素。它也与致癌作用有关，但 RBM24 在膀胱癌 (BC) 中的功能仍不清楚。在本研究中，我们发现 RBM24 在 BC 组织中上调。重要的是，我们发现较高水平的 RBM24 与 BC 患者的不良预后相关。RBM24 的过表达促进了 BC 细胞增殖，而 RBM24 的消耗抑制了体内和体外的 BC 细胞增殖。从机制上讲，RBM24 通过结合并增强 Runx1t1 mRNA 的稳定性，正向调节 BC 细胞中的 Runx1t1 表达。此外，Runx1t1 反过来通过与转录因子 TCF4 相互作用并抑制直接靶向 RBM24 并抑制 RBM24 表达的 miR-625-5p 的转录来促进 RBM24 表达。RBM24 调节的 BC 细胞增殖通过 Runx1t1/TCF4/miR-625-5p 反馈回路调节。这些结果表明 RBM24/Runx1t1/TCF4/miR-625-5p 正反馈回路参与 BC 进展。破坏该途径可能是 BC 治疗的潜在治疗策略。