依赖于 m6A 的成熟 miR-151-5p 通过靶向 LYPD3 加速了 HNSCC 的恶性进程。

IF 6.3 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular biomedicine Pub Date : 2024-07-16 DOI:10.1186/s43556-024-00189-9
Fei Huang, Yuan Ren, Yufei Hua, Ying Wang, Ruomeng Li, Ning Ji, Xin Zeng, Ding Bai, Qianming Chen, Xikun Zhou, Junjie Wu, Jing Li
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引用次数: 0

摘要

miRNA 已成为各种病理和生理过程中的重要调节因子,但其确切的作用机制仍不完全清楚。本研究揭示了 mi-151-5p 在肿瘤细胞中的作用,发现它在肿瘤细胞中的表达明显升高,这显著增强了 HNSCC 细胞的侵袭和迁移。这种作用是通过 miR-151-5p 直接靶向 LY6/PLAUR Domain Containing 3 (LYPD3),与 LYPD3 mRNA 中的 3'- 非翻译区 (3'-UTR) 互补结合实现的。因此,这种相互作用加速了 HNSCC 的转移。值得注意的是,临床观察表明,miR-151-5p 的高表达和 LYPD3 的低水平与 HNSCC 患者的不良预后相关。此外,我们的研究表明,LYPD3 的糖基化可调节其亚细胞定位,并加强其抑制 HNSCC 转移的作用。此外,我们还发现了一种潜在的调控机制,即通过 N6-甲基腺苷(m6A)修饰促进 miR-151-5p 的成熟和积累。这一过程由类似甲基转移酶 3(METTL3)协调,并由新发现的阅读器异质核糖核蛋白 U(hnRNP U)介导。这些发现共同强调了METTL3/miR-151-5p/LYPD3轴在HNSCC恶性进展中的重要作用。
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m6A-dependent mature miR-151-5p accelerates the malignant process of HNSCC by targeting LYPD3.

miRNA has emerged as a crucial regulator in various of pathological and physiological processes, yet its precise mechanism of action the detailed mechanism of their action in Head and neck squamous cell carcinoma (HNSCC) remains incompletely understood. This study sheds light on the role of mi-151-5p, revealing its significantly elevated expression in tumor cells, which notably enhances the invasion and migration of HNSCC cells. This effect is achieved through directly targeting LY6/PLAUR Domain Containing 3 (LYPD3) by miR-151-5p, involving complementary binding to the 3'-untranslated regions (3'-UTR) in the mRNA of LYPD3. Consequently, this interaction accelerates the metastasis of HNSCC. Notably, clinical observations indicate a correlation between high expression of miR-151-5p and low levels of LYPD3 in clinical settings are correlated with poor prognosis of HNSCC patients. Furthermore, our investigation demonstrates that glycosylation of LYPD3 modulates its subcellular localization and reinforces its role in suppressing HNSCC metastasis. Additionally, we uncover a potential regulatory mechanism involving the facilitation of miR-151-5p maturation and accumulation through N6-methyladenosine (m6A) modification. This process is orchestrated by methyltransferase-like 3 (METTL3) and mediated by a newly identified reader, heterogeneous nuclear ribonucleoprotein U (hnRNP U). These findings collectively underscore the significance of the METTL3/miR-151-5p/LYPD3 axis serves as a prominent driver in the malignant progression of HNSCC.

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