State Key Laboratory of Pharmaceutical Biotechnology, Drum Tower Hospital Affiliated to Medical School, School of Life Sciences, Nanjing University, Nanjing 210023, China.
Department of Hematology, Drum Tower Hospital Affiliated to Medical School, Nanjing University, Nanjing 210008, China.
Nucleic Acids Res. 2024 Oct 14;52(18):10810-10822. doi: 10.1093/nar/gkae788.
RNA-binding proteins (RBPs) are attractive targets in human pathologies. Despite a number of efforts to target RBPs with small molecules, it is still difficult to develop RBP inhibitors, asking for a deeper understanding of how to chemically perturb RNA-binding activity. In this study, we found that the thiopurine drugs (6-mercaptopurine and 6-thioguanine) effectively disrupt CELF1-RNA interaction. The disrupting activity relies on the formation of disulfide bonds between the thiopurine drugs and CELF1. Mutating the cysteine residue proximal to the RNA recognition motifs (RRMs), or adding reducing agents, abolishes the disrupting activity. Furthermore, the 1,2,4-triazole-3-thione, a thiopurine analogue, was identified with 20-fold higher disrupting activity. Based on this analogue, we found that compound 9 disrupts CELF1-RNA interaction in living cells and ameliorates CELF1-mediated myogenesis deficiency. In summary, we identified a thiol-mediated binding mechanism for thiopurine drugs and their derivatives to perturb protein-RNA interaction, which provides novel insight for developing RBP inhibitors. Additionally, this work may benefit the pharmacological and toxicity research of thiopurine drugs.
RNA 结合蛋白(RBPs)是人类病理学中的一个有吸引力的靶点。尽管已经做了很多努力,试图用小分子来靶向 RBPs,但开发 RBP 抑制剂仍然很困难,这就需要我们更深入地了解如何用化学方法干扰 RNA 结合活性。在这项研究中,我们发现硫嘌呤类药物(6-巯基嘌呤和 6-硫鸟嘌呤)能有效地破坏 CELF1-RNA 相互作用。这种破坏活性依赖于硫嘌呤类药物与 CELF1 之间形成二硫键。突变靠近 RNA 识别基序(RRMs)的半胱氨酸残基,或添加还原剂,会使破坏活性丧失。此外,我们还鉴定出一种硫嘌呤类似物 1,2,4-三唑-3-硫酮,其破坏活性高 20 倍。基于这个类似物,我们发现化合物 9 可以破坏活细胞中 CELF1-RNA 的相互作用,并改善 CELF1 介导的成肌细胞缺陷。总之,我们确定了硫嘌呤类药物及其衍生物通过巯基介导的结合机制来干扰蛋白质-RNA 相互作用,这为开发 RBP 抑制剂提供了新的思路。此外,这项工作可能有益于硫嘌呤类药物的药理学和毒性研究。