RNA-binding proteins (RBPs) play critical roles in regulating post-transcriptional gene expression, managing processes such as mRNA splicing, stability, and translation. In normal intestine, RBPs maintain the tissue homeostasis, but when dysregulated, they can drive colorectal cancer (CRC) development and progression. Understanding the molecular mechanisms behind CRC is vital for developing novel therapeutic strategies, and RBPs are emerging as key players in this area. This review highlights the roles of several RBPs, including LIN28, IGF2BP1–3, Musashi, HuR, and CELF1, in CRC. These RBPs regulate key oncogenes and tumor suppressor genes by influencing mRNA stability and translation. While targeting RBPs poses challenges due to their complex interactions with mRNAs, recent advances in drug discovery have identified small molecule inhibitors that disrupt these interactions. These inhibitors, which target LIN28, IGF2BPs, Musashi, CELF1, and HuR, have shown promising results in preclinical studies. Their ability to modulate RBP activity presents a new therapeutic avenue for treating CRC. In conclusion, RBPs offer significant potential as therapeutic targets in CRC. Although technical challenges remain, ongoing research into the molecular mechanisms of RBPs and the development of selective, potent, and bioavailable inhibitors should lead to more effective treatments and improved outcomes in CRC.
RNA结合蛋白（RBPs）在转录后基因表达的调控中发挥关键作用，参与mRNA剪接、稳定性维持及翻译等过程。在正常肠道组织中，RBPs维持组织稳态；而当其功能失调时，则会驱动结直肠癌（CRC）的发生与发展。深入理解CRC的分子机制对开发新型治疗策略至关重要，而RBPs正逐渐成为该领域的关键调控因子。本综述重点探讨了LIN28、IGF2BP1–3、Musashi、HuR及CELF1等多种RBPs在CRC中的作用机制。这些蛋白通过调控mRNA稳定性与翻译过程，影响关键癌基因和抑癌基因的表达。尽管RBPs因其与mRNA的复杂相互作用而难以靶向，但药物研发领域的最新进展已发现可破坏此类相互作用的小分子抑制剂。针对LIN28、IGF2BPs、Musashi、CELF1和HuR的抑制剂在临床前研究中展现出良好前景，其调控RBP活性的能力为CRC治疗提供了新方向。总之，RBPs作为CRC治疗靶点具有重要潜力。尽管仍存在技术挑战，但通过对RBP分子机制的持续探索，以及开发选择性高、效力强且生物可利用性好的抑制剂，有望为CRC提供更有效的治疗方案并改善患者预后。
RNA Binding Proteins as Potential Therapeutic Targets in Colorectal Cancer
肿瘤(癌症)患者之家