{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐411 is a multifunctional microRNA whose role in cancer is highly context‐dependent. In some malignancies such as lung adenocarcinoma, non–small cell lung cancer, hepatocellular carcinoma and certain breast and ovarian cancers, elevated levels of miR‐411 (or its −5p/−3p isoforms) promote cell proliferation, migration and invasion through the downregulation of tumor‐suppressor targets (e.g. FOXO1, ITCH, SPRY4, TXNIP, and GRB2), while in other cancers such as breast, ovarian and glioblastoma, its reduced expression is associated with tumor progression and poorer prognosis. In addition, modifications such as RNA editing and isomiR formation can shift its seed sequence and target spectrum, thereby influencing key oncogenic pathways such as MAPK and PI3K/AKT signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct roles in tumor cell behavior, miR‐411 is intricately involved in regulatory networks mediated by noncoding RNAs and in a spectrum of nonmalignant conditions. For example, several studies have documented that circular RNAs (such as circ_001569, circ_000926, and circ_0082182) and long noncoding RNAs (including CDKN2B‐AS1, PCED1B‐AS1, and ANRIL) can bind and “sponge” miR‐411, thereby altering its availability and modulating downstream targets that affect epithelial–mesenchymal transition, cell invasion, and drug sensitivity. Beyond oncogenesis, roles for miR‐411 have been reported in vascular contexts—as a 5′‐isomiR influencing post‐ischemic neovascularization—as well as in diseases such as osteoarthritis, diabetic retinopathy and preeclampsia, where changes in miR‐411 levels impact processes like autophagy and trophoblast function by targeting molecules including HIF‐1α and PTEN."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "25"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these findings—as further reviewed by recent analyses—underscore the dualistic nature of miR‐411 in disease. In some contexts, such as certain NSCLC subtypes and head and neck squamous cell carcinoma, miR‐411 overexpression (or alterations via RNA editing) can promote oncogenic processes and modulate therapeutic response (for example, by targeting MET and attenuating MAPK activity), whereas in other scenarios, such as glioblastoma and cervical cancer, miR‐411 acts as a tumor suppressor by engaging targets like STAT3 and STK17A and activating pro‐apoptotic pathways. This broad spectrum of regulatory interactions positions miR‐411 as a promising biomarker for diagnosis, prognosis and even as a potential therapeutic target across multiple disease settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "31"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Naoe Harafuji, Peter Schneiderat, Maggie C Walter, et al. 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