{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMINCR is a long non‐coding RNA transcriptionally induced by MYC that plays a pivotal role in controlling cell cycle progression. In MYC‐driven tumors such as Burkitt lymphoma, MINCR enhances MYC’s binding to promoters of key cell cycle regulators – including Aurora kinases and factors involved in DNA replication licensing – thus reinforcing the MYC transcriptional network. Moreover, MINCR has been shown to act as a molecular sponge for several microRNAs, fine‐tuning the expression levels of downstream targets."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in modulating MYC activity, MINCR is overexpressed in a diverse array of cancers—including gallbladder cancer, non‐small cell lung cancer, oral squamous cell carcinoma, glioma, osteosarcoma, and colon cancer—where it exerts potent oncogenic functions. It promotes tumor progression and metastasis by functioning as a competing endogenous RNA: for example, MINCR sequesters miR‑26a‑5p to upregulate EZH2, modulates the miR‑126/SLC7A5 axis in lung cancer, and sponges miR‑876‑5p to relieve suppression on GSPT1 in glioma. Furthermore, activation of the Wnt/β‑catenin pathway by MINCR has been implicated in enhanced proliferation, epithelial–mesenchymal transition and invasive behavior."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, dysregulated (often overexpressed) MINCR levels correlate with aggressive tumor parameters and poor prognosis. In hepatocellular carcinoma and non‐small cell lung cancer, for instance, elevated MINCR expression has been linked to increased tumor volume, lymph node metastasis, and reduced overall survival. Additional studies have investigated its relationship with key cell cycle mediators such as Cyclin‐dependent kinase 2 and its potential modulation of signaling axes such as the microRNA‑107/β‑catenin pathway, underscoring its promise both as a prognostic biomarker and as a potential therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Gero Doose, Andrea Haake, Stephan H Bernhart, et al. 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