{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR100HG is a long non‐coding RNA that serves as a host gene for several microRNAs—including miR‑100, miR‑125b, and let‑7a—yet it also functions independently to regulate key cellular processes. Although its role as the precursor for these miRNAs was noted early on, its own transcript‐mediated activities remain multifaceted. In neuronal contexts, for example, the related linc‐NeD125 regulates cell proliferation and resistance to apoptosis, while broader studies have linked MIR100HG with the modulation of cell proliferation, apoptosis, cell cycle progression and differentiation through its associations with major signaling pathways such as TGF‑β, Wnt, Hippo, and ERK/MAPK."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn several solid tumors, MIR100HG acts as an oncogene. In triple‑negative breast cancer, its overexpression promotes cell proliferation by regulating p27 and forming RNA–DNA triplexes, while in osteosarcoma and gastric cancer high MIR100HG levels correlate with increased tumor cell proliferation, invasion and poor patient prognosis. Similarly, in lung cancer and nasopharyngeal carcinoma, MIR100HG facilitates proliferation and metastasis through axes involving miR‑5590‑3p/DCBLD2 and miR‑136‑5p/IL‑6, respectively."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMIR100HG is also intricately involved in the regulation of the cell cycle and epithelial‐to‐mesenchymal transition. In pancreatic ductal adenocarcinoma, TGF‑β induces its transcription via SMAD2/3, thereby coordinating the expression of its embedded microRNAs—specifically, the pro‑tumorigenic miR‑100 and miR‑125b, while concurrently leaving anti‑tumorigenic let‑7a levels unchanged due to LIN28B‐mediated processing inhibition. Moreover, independent of its miRNAs, a stable, spliced nuclear isoform of MIR100HG modulates cell cycle progression by facilitating the interaction between the RNA binding protein HuR and its target mRNAs."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn colorectal carcinoma, MIR100HG is subject to transcriptional repression by β‑catenin. Here, reduced MIR100HG levels correlate with decreased histone H3K27 acetylation on its promoter via HDAC6 recruitment. Functionally, overexpressing MIR100HG induces G0‑G1 arrest through upregulation of the cell cycle inhibitor p57, suggesting a context‑dependent, tumor‑suppressive role, although its overall contributions to cetuximab resistance remain to be fully elucidated."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Stephan Emmrich, Alexandra Streltsov, Franziska Schmidt, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "LncRNA MIR100HG promotes cell proliferation in triple-negative breast cancer through triplex formation with p27 loci."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Dis (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41419-018-0869-2"}], "href": "https://doi.org/10.1038/s41419-018-0869-2"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30042378"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30042378"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Xiaochuan Su, Junyan Teng, Guoguo Jin, et al. "}, {"type": "b", "children": [{"type": "t", "text": "ELK1-induced upregulation of long non-coding RNA MIR100HG predicts poor prognosis and promotes the progression of osteosarcoma by epigenetically silencing LATS1 and LATS2."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biomed Pharmacother (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.biopha.2018.10.029"}], "href": "https://doi.org/10.1016/j.biopha.2018.10.029"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30551532"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30551532"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Jun Li, Qingfeng Xu, Wen Wang, et al. 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