{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have established that terminal differentiation‐inducing non‐protein coding RNA (TINCR) is a multifunctional regulator of cell fate. Initially characterized in human epidermal keratinocytes, TINCR was shown to bind a specific 25‐nucleotide “TINCR box” motif in differentiation‐associated mRNAs and interact with RNA‐binding proteins such as Staufen1, thereby stabilizing transcripts essential for terminal differentiation and tissue homeostasis. In addition, TINCR has been implicated in broader physiologic contexts including the regulation of keratinocyte cornification via its encoded microprotein (TUBL), as well as in cardiac and dermal cells and trophoblasts where it modulates epigenetic programs and stress‐related signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTINCR also exhibits striking context‐dependent functions in cancer. In gastrointestinal malignancies such as gastric and colorectal cancer, TINCR expression can be either upregulated or lost, with the former driving oncogenic processes via E2F1‐mediated transcriptional induction and modulation of mRNA stability, and the latter associating with aggressive progression and radioresistance through mechanisms involving microRNA sponging (e.g. of miR‑137) and consequent regulation of critical targets including CD36 and TCF4. In addition, in cancers of the lung, breast, bladder, nasopharynx, esophagus, and cervix, TINCR has been shown to promote proliferation, invasion, and chemoresistance by engaging distinct molecular partners—ranging from direct binding to oncoproteins such as BRAF and regulators of the cell cycle (e.g. CDK6) to acting as a competing endogenous RNA for various microRNAs (for example, miR‑503‑5p, miR‑29c, and miR‑302). Moreover, in hematologic malignancies, TINCR contributes to the stabilization of endogenous retroviral RNA as part of a Staufen1‐containing ribonucleoprotein complex that influences therapeutic responses to DNA‐methyltransferase inhibitors. Collectively, these findings underscore a dual role for TINCR in cancer, with genetic polymorphisms further modulating its expression and clinical impact."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cell differentiation and oncogenesis, TINCR is emerging as a context‐dependent modulator of cellular stress responses and therapeutic outcomes. Some reports suggest that its dysregulation may have minimal impact in certain settings—for example, in pituitary null cell adenomas—while in other contexts, altered TINCR expression contributes to chemoresistance (as in choroidal melanoma) or influences sensitivity to targeted immunotherapies through regulation of PD‑L1. In parallel, unresolved questions regarding its involvement in diabetic cardiomyopathy and additional non‐cancerous conditions reflect the complex interplay of TINCR with epigenetic modifiers and RNA‐binding proteins. Such controversies and gaps in our understanding are highlighted by studies that report limited or context‐specific roles for TINCR."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "38", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Markus Kretz, Zurab Siprashvili, Ci Chu, et al. 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