{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nFAM83H‐AS1 has emerged as a broadly dysregulated long noncoding RNA in human malignancies, with a recurrent oncogenic role demonstrated in pan‐cancer analyses. It is overexpressed in diverse tumor types including cervical, ovarian, lung, glioma, bladder, colon, hepatocellular, gastric, and endometrial cancers, where its elevated levels correlate with advanced clinical stage, increased metastasis, resistance to chemo‐ or radiotherapy, and overall poorer patient outcomes. In cervical cancer, for instance, FAM83H‐AS1 expression promotes cell proliferation and migration, while in lung adenocarcinoma and ovarian cancer its upregulation is linked to enhanced tumor progression and aberrant signaling activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, FAM83H‐AS1 exerts its oncogenic functions via multiple pathways. In several studies it has been shown to regulate critical cell cycle and survival processes by epigenetically silencing tumor suppressors – for example, its recruitment of EZH2 leads to suppression of CDKN1A in glioma, while in endometrial cancer it recruits DNMT1 to promote hypermethylation of the CDO1 promoter and inhibit ferroptosis. Furthermore, FAM83H‐AS1 influences key signaling pathways; it modulates MET/EGFR signaling in lung cancer and impedes TGF‐β signaling in colon cancer through downregulation of SMAD proteins. At the post‐transcriptional level, m6A modifications mediated by factors such as WTAP, METTL3, and IGF2BP2/3 have been implicated in enhancing FAM83H‐AS1 RNA stability, and the RNA binding protein PTBP1 has been identified as critical for its function in colorectal cancer. In addition, FAM83H‐AS1 can act as a competing endogenous RNA by sponging microRNAs (e.g., miR‐541‐3p), thereby modulating downstream targets like WNT3A and promoting oncogenic as well as differentiation‐related processes in both cancer and non‐cancer contexts (e.g., osteogenic differentiation in osteomyelitis and cell growth in intervertebral disc degeneration)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_fs", "start_ref": "11", "end_ref": "14"}, {"type": "fg_f", "ref": "10"}, {"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe multifaceted roles of FAM83H‐AS1 underscore its potential as both a prognostic biomarker and a therapeutic target. Functional inhibition via knockdown or antisense oligonucleotides has been shown to reduce tumor cell proliferation, migration, invasion, and resistance phenomena, thereby enhancing apoptosis and cell cycle arrest in various preclinical models. These therapeutic benefits, combined with its regulatory impact on oncogenic signaling and epigenetic modifications, position FAM83H‐AS1 as a promising candidate for targeted interventions across an array of cancers as well as disorders of tissue differentiation and degeneration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Christopher R Cabanski, Nicole M White, Ha X Dang, et al. 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