有证据表明，小核糖核酸（snoRNAs）参与肿瘤发生和发展，并可能成为结直肠癌（CRC）的有希望的生物标志物。在这里，我们检查了CRC中snoRNAs的表达谱，并发现SNORD11B在CRC肿瘤组织和细胞系中的表达增加，SNORD11B的表达与其宿主基因NOP58之间存在显著的正相关性。SNORD11B促进CRC细胞增殖和侵袭，抑制细胞凋亡。在机制上，SNORD11B通过在18S核糖体RNA（rRNA）的G509位点介导2'-O-甲基化（Nm）修饰，促进18S rRNA的处理和成熟。有趣的是，SNORD11B通过一个典型的基序介导了MIRLET7A1HG（pri-let-7a）的G225位点上的Nm修饰，导致pri-let-7a的降解，DGCR8结合的抑制，成熟肿瘤抑制基因let-7a-5p的表达减少以及下游致癌基因的上调翻译。SNORD11B在CRC的诊断上与CEA和CA199相比具有可比性。SNORD11B的高表达与更晚期的TNM分期和淋巴结转移显著相关，预示着不良预后。© 2023. 作者授予施普林格自然出版集团独家许可使用。

Evidence indicates that small nucleolar RNAs (snoRNAs) participate in tumorigenesis and development and could be promising biomarkers for colorectal cancer (CRC). Here, we examine the profile of snoRNAs in CRC and find that expression of SNORD11B is increased in CRC tumor tissues and cell lines, with a significant positive correlation between SNORD11B expression and that of its host gene NOP58. SNORD11B promotes CRC cell proliferation and invasion and inhibits apoptosis. Mechanistically, SNORD11B promotes the processing and maturation of 18 S ribosomal RNA (rRNA) by mediating 2'-O-methylated (Nm) modification on the G509 site of 18 S rRNA. Intriguingly, SNORD11B mediates Nm modification on the G225 site of MIRLET7A1HG (pri-let-7a) with a canonical motif, resulting in degradation of pri-let-7a, inhibition of DGCR8 binding, reduction in mature tumor suppressor gene let-7a-5p expression, and upregulation of downstream oncogene translation. SNORD11B performs comparably to CEA and CA199 in diagnosing CRC. High expression of SNORD11B is significantly correlated with a more advanced TNM stage and lymph node metastasis, which indicates poor prognosis.© 2023. The Author(s), under exclusive licence to Springer Nature Limited.