{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nX‐inactivation in female mammals is orchestrated by the long non‐coding RNA XIST, which initiates transcriptional silencing in cis by coating one X chromosome and recruiting a host of chromatin‐modifying factors. Structural domains—including its evolutionarily conserved A‐repeat region—and post‑transcriptional modifications such as N6‑methyladenosine (m6A) deposition (mediated by RBM15/15B and METTL3, and recognized by YTHDC1) are critical for establishing and maintaining this silenced state. Moreover, XIST engages with multiple proteins during its assembly into a ribonucleoprotein complex that governs chromatin remodeling and epigenetic repression."}, {"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": "\nBeyond its canonical role in dosage compensation, aberrant XIST expression has been widely reported in diverse human malignancies. In several cancers—including testicular germ cell tumors, breast, glioblastoma, non‑small cell lung, pancreatic, colorectal, bladder, thyroid, and colon cancers—altered levels of XIST are associated with dysregulated cell proliferation, migration, invasion, epithelial–mesenchymal transition, metastasis, and even chemoresistance. Mechanistically, XIST is often found to function as a competing endogenous RNA (ceRNA) that sponges specific microRNAs (such as miR‑152, miR‑92b, miR‑200b‑3p, miR‑34a, miR‑21‑5p, among others) thereby modulating the expression of key oncogenes or tumor suppressors (for example, KLF2, SMAD7, E2F3, PDCD4) and influencing critical signaling pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in epigenetic silencing and tumorigenesis, XIST participates in a broader network of cellular processes. It contributes to the regulation of stem cell pluripotency and differentiation by interfacing with epitranscriptomic regulators, thereby modulating the m6A landscape on key messenger RNAs. XIST also influences immune cell function and has been implicated in non‑cancer pathologies such as myocardial injury, osteoarthritis, and acute kidney injury. Through its capacity to interact with microRNAs and various RNA‑binding proteins, XIST integrates transcriptional and post‑transcriptional regulatory mechanisms to fine‑tune gene expression programs across a spectrum of developmental and disease contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "L B Herzing, J T Romer, J M Horn, et al. 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