结直肠癌（CRC）通常由腺瘤缓慢发展，但其潜在机制尚不清楚，这妨碍了结直肠腺瘤-癌进展的预防或治疗。在本研究中，我们使用深入的定量蛋白质组学结合生存分析，揭示核仁蛋白U3小核糖核酸相关蛋白18同源物（UTP18）在结直肠腺瘤转化为癌症过程中持续上调，并与腺瘤复发、有效的血清诊断以及CRC的不良预后相关。此外，去SUMO化诱导UTP18的核质转运，通过调节p21 mRNA的不稳定性推动细胞周期进展和肿瘤发生。此外，过表达UTP18促进腺瘤器官样体的生长和核糖体生物合成。因此，UTP18在肿瘤发生和恶变中发挥多种作用，表明它可能是结直肠腺瘤和癌症的潜在生物标志物和药物靶点。版权所有©2023作者。 Elsevier Inc.保留所有权利。

Colorectal cancer (CRC) often develops slowly from adenoma, but the underlying mechanism remains unclear, hampering the prevention or treatment of colorectal adenoma-carcinoma progression. In this study, we use in-depth quantitative proteomics combined with survival analysis, revealing that the ribosome protein U3 small nucleolar RNA-associated protein 18 homolog (UTP18) is consistently upregulated in the progression of colorectal adenoma to carcinoma and is associated with adenoma recurrence, effective serodiagnosis, and poor prognosis of CRC. Furthermore, deSUMOylation induces the nucleocytoplasmic transport of UTP18, driving cell-cycle progression and tumorigenesis via mediation of the instability of p21 mRNA. In addition, the growth and ribosome biogenesis of adenoma organoids is found to be promoted by overexpression of UTP18. Thus, UTP18 contributes to multiple roles in adenogenesis and malignancy of CRC, suggesting that it could be a potential biomarker and drug target for colorectal adenoma and cancer.Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.