{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑1290 is emerging as a multifunctional microRNA that plays an oncogenic role in a variety of human cancers. In several studies, its aberrant expression has been linked to tumor initiation, progression, and metastasis in malignancies such as non‑small cell lung cancer, colorectal cancer, esophageal squamous cell carcinoma, pancreatic cancer, breast cancer, and laryngeal squamous cell carcinoma. Mechanistically, miR‑1290 targets multiple regulators—including IRF2, NAT1, INPP4B, FOXA1, NKD1, and others—to promote cell proliferation, epithelial–mesenchymal transition, invasion, and delayed cytokinesis. In addition, its circulating levels, detected in plasma or within extracellular vesicles, have shown promise as non‑invasive biomarkers when combined with established markers (for example, CA 19‑9) for the early detection and monitoring of pancreatic and gastrointestinal cancers, as well as in selecting high‑risk patients for surveillance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncogenic functions, miR‑1290 has been implicated in non‑cancer biological processes. In neuronal systems, for example, it is upregulated during differentiation and can be transferred via endothelial‑derived extracellular vesicles to protect neurons against ischemic injury—effects that involve modulation of key cell cycle proteins and regulators such as HIF‑3α. In addition, miR‑1290 participates in the regulation of HIV‑1 latency by interacting with the viral 3′‑UTR and modulating host factors, and it influences myoblast differentiation and muscle atrophy. In inflammatory conditions, such as psoriasis, increased miR‑1290 release from neutrophils correlates with disease severity by promoting keratinocyte proliferation. These observations underscore its diverse roles in cellular differentiation, survival, and inflammatory responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "10"}, {"type": "fg_fs", "start_ref": "21", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMiR‑1290 is also a critical node within complex regulatory networks that extend its influence across multiple disease contexts. It has been shown to modulate the brain metastatic microenvironment in breast cancer by activating astrocytes via a FOXA2–CNTF signaling axis, while in chordoma and laryngeal cancer it participates in ceRNA networks that affect tumor invasion and apoptosis. In prostate cancer, miR‑1290 targets transcription factors such as RORA to promote a malignant phenotype and can determine sensitivity to radiation therapy in aggressive triple‑negative breast cancers. Its interactions with circular RNAs and long non‑coding RNAs—in cancers like esophageal carcinoma and endometrial cancer—further affect key pathways such as PI3K/Akt and Wnt/β‑catenin, thereby modulating epithelial–mesenchymal transition. In addition, miR‑1290 has been linked to the regulation of drug‐metabolizing enzymes (NAT1/NAT2) and may influence endothelial-to‑mesenchymal transition relevant to vascular remodeling. Collectively, these findings illustrate the multifaceted nature of miR‑1290 as both a mechanistic driver and a potential diagnostic and therapeutic target in oncologic and non‑oncologic diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yongliang Zhu, Qiaoli Jiang, Xiaojun Lou, et al. 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