{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIR615 is expressed as two mature strands—miR‐615‑5p and miR‐615‑3p—that serve as versatile regulators in diverse diseases. In several cancers and vascular pathologies, the miR‐615‑5p arm frequently functions as a tumor suppressor. It is downregulated in non–small cell lung cancer, pancreatic ductal adenocarcinoma, hepatocellular carcinoma, esophageal squamous cell carcinoma, glioblastoma, and related malignancies, where its loss promotes proliferation, migration, angiogenesis, and metastasis by failing to restrain targets such as insulin‐like growth factor‐2 (IGF2), SHMT2, EGFR, and downstream effectors of VEGF–AKT/eNOS signaling. Upstream transcription factors like CDX2 and PU.1 enhance miR‐615‑5p expression, further enforcing its inhibition of oncogenic drivers and mitigating tumor cell invasion and immune‐cell deregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast, the miR‐615‑3p arm displays context‐dependent roles that can be oncogenic or influence differentiation processes. In gastric, prostate, and ovarian cancers, for example, miR‐615‑3p is often overexpressed and linked to enhanced cell viability, proliferation, migration, and telomerase activity—functions attributed to the suppression of targets such as CELF2 and cyclin D2. Beyond its involvement in tumor biology, miR‐615‑3p also regulates normal cellular processes. It modulates the osteogenic differentiation of ligament cells via direct repression of FOXO1 and GDF5, augments the phagocytic capacity of splenic macrophages by downregulating LCoR (thereby derepressing PPARγ), and contributes to cardiomyocyte responses in oxidative stress and apoptosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA further layer of complexity arises from the regulation of MIR615 by various long noncoding and circular RNAs. In multiple tumor types, oncogenic long noncoding RNAs (such as HOTTIP and Gm15290) and circular RNAs (including circRNA 100146, circZNF609, circ_002144, circ-PITX1, and circ_0004396) act as molecular sponges to sequester miR‐615, thereby abrogating its tumor‐suppressive activities and de‐repressing targets like IGF2, AKT2, LARP1, and SMARCE1. Moreover, epigenetic modifications—such as promoter hypermethylation—further downregulate miR‐615 expression in some contexts, exacerbating oncogenic signaling. Together, these regulatory networks underscore the pivotal role of MIR615 as a nodal mediator whose precise function depends on its strand, cellular context, and interplay with other noncoding RNAs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lijian Chen, Aruo Nan, Nan Zhang, et al. 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