{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMaternally expressed gene 3 (MEG3) is an imprinted long non‐coding RNA with potent tumor‐suppressive properties that have been documented in a wide range of human cancers. Reduced MEG3 expression—frequently resulting from promoter hypermethylation—has been correlated with enhanced cell proliferation, reduced apoptosis, and more aggressive phenotypes in tumors such as pituitary adenomas, meningiomas, hepatocellular carcinoma, glioma, bladder, cervical, gastric, colorectal, breast, lung, and prostate cancers. In these studies, forced re‐expression of MEG3 led to increased p53 protein levels and p53‐dependent transcriptional activation, cell cycle arrest, and induction of apoptosis, while MEG3’s function as a competing endogenous RNA (ceRNA) helped sequester oncogenic microRNAs. Collectively, these findings not only underscore MEG3’s role in maintaining normal cellular growth control but also highlight its potential value as a prognostic biomarker and therapeutic target in oncology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistic studies have provided further insight into how MEG3 governs cellular behavior. Environmental stimuli such as prenatal famine exposure and nickel have been shown to induce hypermethylation at the MEG3 promoter, thereby silencing its expression. Detailed investigations into RNA structure revealed that evolutionarily conserved tertiary motifs—including alternative pseudoknot “kissing-loop” formations—are critical for MEG3’s ability to interact with transcription factors and chromatin modifiers. Through formation of RNA–DNA triplexes, MEG3 guides epigenetic complexes (for example, those involving polycomb repressive complex components) to target gene promoters, thereby modulating histone methylation and gene transcription. These epigenetic and structural mechanisms are essential for mediating its effects on p53 activation and downstream tumor‐suppressive transcriptional programs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐established role in tumor suppression, MEG3 participates in a variety of non‐neoplastic processes. Altered MEG3 expression has been linked to metabolic disease risk—including associations with type 1 and type 2 diabetes—and plays a role in the balance of osteogenic and adipogenic differentiation of mesenchymal and adipose‐derived stromal cells, in part by modulating factors such as BMP4. MEG3 also regulates autophagy and inflammatory responses in contexts ranging from mycobacterial infection to osteoarthritis and ischemic brain injury, while dysregulation in trophoblasts has been implicated in preeclampsia. These diverse functions underscore the broad biological significance of MEG3 and suggest that restoring its expression or function may offer novel therapeutic avenues not only in cancers but also in metabolic, musculoskeletal, and inflammatory disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "44"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "N Miyoshi, H Wagatsuma, S Wakana, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Identification of an imprinted gene, Meg3/Gtl2 and its human homologue MEG3, first mapped on mouse distal chromosome 12 and human chromosome 14q."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes Cells (2000)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1046/j.1365-2443.2000.00320.x"}], "href": "https://doi.org/10.1046/j.1365-2443.2000.00320.x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "10759892"}], "href": "https://pubmed.ncbi.nlm.nih.gov/10759892"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Xun Zhang, Yunli Zhou, Kshama R Mehta, et al. 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