Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Inflammatory Bowel Disease Research Center. Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 160# Pu Jian Ave, Shanghai 200127, China; Shanghai Institute of Digestive Disease, China.
Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Inflammatory Bowel Disease Research Center. Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 160# Pu Jian Ave, Shanghai 200127, China; Shanghai Institute of Digestive Disease, China.
J Adv Res. 2023 Apr;46:75-85. doi: 10.1016/j.jare.2022.06.004. Epub 2022 Jun 11.
Previous studies have focused on the involvement of small nucleolar RNAs (snoRNAs) and SNHGs in tumor cell proliferation, apoptosis, invasion, and metastasis via multiple pathways, including phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT), Wnt/β catenin, and mitogen-activated protein kinase (MAPK). These molecular mechanisms affect the integrity of the intestinal mucosal barrier.
Current evidence regarding snoRNAs and SNHGs in the context of the mucosal barrier and modulation of homeostasis is fragmented. In this review, we collate the established information on snoRNAs and SNHGs as well as discuss the major pathways affecting the mucosal barrier.
Intestinal mucosal immunity, microflora, and the physical barrier are altered in non-neoplastic diseases such as inflammatory bowel diseases. Dysregulated snoRNAs and SNHGs may impact the intestinal mucosal barrier to promote the pathogenesis and progression of multiple diseases. SnoRNAs or SNHGs has been shown to be associated with poor disease behaviors, indicating that they may be exploited as prognostic biomarkers. Additionally, clarifying the complicated interactions between snoRNAs or SNHGs and the mucosal barrier may provide novel insights for the therapeutic treatment targeting strengthen the intestinal mucosal barrier.
先前的研究集中于小核仁 RNA(snoRNA)和 SNHG 通过多种途径(包括磷脂酰肌醇-3-激酶/蛋白激酶 B(PI3K/AKT)、Wnt/β 连环蛋白和丝裂原活化蛋白激酶(MAPK))参与肿瘤细胞增殖、凋亡、侵袭和转移。这些分子机制影响肠道黏膜屏障的完整性。
目前关于 snoRNA 和 SNHG 在黏膜屏障和稳态调节方面的证据是零散的。在这篇综述中,我们汇集了关于 snoRNA 和 SNHG 的既定信息,并讨论了影响黏膜屏障的主要途径。
非肿瘤性疾病(如炎症性肠病)中,肠道黏膜免疫、微生物群和物理屏障发生改变。失调的 snoRNA 和 SNHG 可能会影响肠道黏膜屏障,促进多种疾病的发病和进展。已经表明 snoRNA 或 SNHG 与不良的疾病行为有关,表明它们可以作为预后生物标志物加以利用。此外,阐明 snoRNA 或 SNHG 与黏膜屏障之间复杂的相互作用可能为靶向增强肠道黏膜屏障的治疗提供新的见解。