{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐1291 has emerged as an important regulator in various cancers through multiple mechanisms that converge on tumor suppression. In hepatoma cells, miR‐1291 indirectly increases glypican‑3 (GPC3) mRNA levels by repressing the endoplasmic reticulum stress sensor IRE1α, thereby stabilizing GPC3 expression. In renal cell carcinoma, miR‐1291 is markedly downregulated; its restoration inhibits cell proliferation, migration, and invasion by directly targeting SLC2A1 (encoding the GLUT1 protein). In esophageal squamous cell carcinoma, miR‑1291 limits tumor aggressiveness by targeting MUC1, leading to reduced cell invasion and increased apoptosis. In pancreatic cancer models, miR‐1291 suppresses tumorigenesis via a FOXA2‑AGR2 regulatory axis and also alters cellular metabolism by elevating nicotinamide N‑methyltransferase (NNMT) and related metabolites. Moreover, an ERRα–CPT1C axis has been uncovered whereby miR‐1291 indirectly modulates mitochondrial energy metabolism, thereby further contributing to its tumor‑suppressive roles."}, {"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 role in directly restraining oncogenic processes, miR‑1291 also modulates cellular drug handling and shows promise as a diagnostic biomarker. In pancreatic carcinoma cells, for instance, miR‑1291—processed from SNORA34—downregulates ABCC1 (MRP1), a key transporter associated with multidrug resistance, thereby promoting higher intracellular accumulation of chemotherapeutic agents and increased chemosensitivity. Circulating miR‑1291 levels have been examined as non‑invasive biomarkers in several clinical contexts including acute myocardial infarction, where its plasma measurement may forecast disease recurrence, in liver cirrhosis versus hepatocellular carcinoma through potential links with GPC3 production, and even in bullous pemphigoid. Furthermore, emerging associations in acute myeloid leukemia suggest that miR‑1291 may intersect with lncRNA (HCP5)‑related pathogenic mechanisms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditionally, miR‑1291 plays a critical role in fibrotic and tissue remodeling processes. In intrauterine adhesions, elevated miR‑1291 levels contribute to endometrial fibrosis by downregulating ArhGAP29, which in turn dysregulates the RhoA/ROCK1 pathway and promotes epithelial–mesenchymal transition. This mechanism underscores its potential both as a therapeutic target and as a circulating biomarker for fibrotic disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Marion Maurel, Nicolas Dejeans, Saïd Taouji, et al. 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