Baazaoui Narjes, Y Alfaifi Mohammad, Ben Saad Rania, Garzoli Stefania
Central Labs, King Khalid University, AlQura'a, Abha, P.O. Box 960, Saudi Arabia; Biology Department, Faculty of Science, King Khalid University, Abha, Saudi Arabia; Tissue Culture and Cancer Biology Research Laboratory, King Khalid University, Abha 9004, Saudi Arabia.
Biotechnology and Plant Improvement Laboratory, Center of Biotechnology of Sfax, B.P "1177", Sfax 3018, Tunisia.
Neuroscience. 2025 Jan 26;565:487-498. doi: 10.1016/j.neuroscience.2024.12.023. Epub 2024 Dec 14.
Neurodegenerative diseases (ND) are complex diseases of still unknown etiology. Lately, long non-coding RNAs (lncRNAs) have become increasingly popular and implicated in several pathologies as they have several roles and appear to be involved in all biological processes such as cell signaling and cycle control as well as translation and transcription. MEG3 is one of these and acts by binding proteins or directly or competitively binding miRNAs. It has a crucial role in controlling cell death, inflammatory process, oxidative stress, endoplasmic reticulum stress, epithelial-mesenchymal transition and other processes. Recent reports showed that MEG3 is a major driving force of the necrosis phenomena in AD, causing the death of neurons, and its upregulation in cancer patients was linked to tumor suppression. Dysregulation of MEG3 affects neuronal cell death, inflammatory process, smooth muscle cell proliferation and consequently leads to the initiation or the acceleration of the disease. This review examines the current state of knowledge concerning the level of expression and the regulatory function of MEG3 in relation to several NDs. In addition, we examined the relation of MEG3 with neurotrophic factors such as Tumor growth factor β (TGFβ) and its possible mechanism of action. A comprehensive and in-depth analysis of the role of MEG3 in ND could give a clearer picture about the initiation of the process of neuronal death and help develop an alternative therapy that targets MEG3.
神经退行性疾病（ND）是病因仍不明的复杂疾病。近来，长链非编码RNA（lncRNA）越来越受到关注，并与多种病理过程相关，因为它们具有多种作用，似乎参与了所有生物过程，如细胞信号传导和周期控制以及翻译和转录。MEG3就是其中之一，它通过结合蛋白质或直接或竞争性地结合微小RNA（miRNA）发挥作用。它在控制细胞死亡、炎症过程、氧化应激、内质网应激、上皮-间质转化及其他过程中起着关键作用。最近的报告表明，MEG3是阿尔茨海默病（AD）坏死现象的主要驱动力，导致神经元死亡，并且其在癌症患者中的上调与肿瘤抑制有关。MEG3的失调会影响神经元细胞死亡、炎症过程、平滑肌细胞增殖，从而导致疾病的发生或加速。本综述探讨了关于MEG3在几种神经退行性疾病中的表达水平和调节功能的现有知识状态。此外，我们研究了MEG3与神经营养因子如肿瘤生长因子β（TGFβ）的关系及其可能的作用机制。对MEG3在神经退行性疾病中的作用进行全面深入的分析，可以更清楚地了解神经元死亡过程的起始，并有助于开发以MEG3为靶点的替代疗法。
