{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNORAD (also known as LINC00657) is a highly conserved and abundantly expressed long noncoding RNA that is rapidly induced by DNA damage. Its primary canonical role is to preserve genomic stability by sequestering Pumilio family RNA‐binding proteins—thereby preventing their hyper‐active repression of mRNAs involved in mitosis, DNA repair, and replication. Notably, NORAD’s repetitive sequence architecture enables it to bind multiple PUM molecules and even drive the formation of phase‐separated “NP bodies” that help modulate RNA–protein interactions critical for genome maintenance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its genome‐stabilizing function, NORAD plays diverse regulatory roles in disease. In a wide array of cancers—including pancreatic, breast, gastric, lung, cervical, hepatocellular, prostate, colorectal, osteosarcoma, and melanoma—dysregulated NORAD expression is associated with altered cell proliferation, epithelial–mesenchymal transition, invasion, metastasis, and even resistance to chemotherapeutic or radiotherapeutic agents. Mechanistically, NORAD functions as a competitive endogenous RNA (ceRNA) that sponges various microRNAs (for example, miR‑608, miR‑136‑5p, miR‑202‑5p, miR‑590‑3p, among others), thereby indirectly regulating key downstream targets and signaling pathways (such as TGF‑β, Wnt/β‑catenin, and autophagy or inflammatory responses) that control tumor growth and stress responses. 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