• Narjes Baazaoui, Y AlfaifiMohammadMCentral 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 Univ, Rania Ben Saad, and Stefania Garzoli.
• 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.
• Neuroscience. 2025 Jan 26; 565: 487498487-498.

AbstractNeurodegenerative 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.Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

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