{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐505 has emerged as a multifaceted regulator in cancer, with its expression frequently altered across tumor types. In several malignancies—including endometrial, cervical, colorectal, hepatocellular, non‐small cell lung, prostate, pancreatic, osteosarcoma, and glioblastoma—miR‐505 generally functions as a tumor suppressor. Its down‐regulation has been linked to enhanced cell proliferation, migration, invasion, and epithelial–mesenchymal transition, whereas in certain contexts (for example, lung adenocarcinoma) its up‐regulation appears to promote oncogenic properties via inhibition of apoptosis. At the molecular level, miR‐505 exerts its effects through direct targeting of key oncogenic transcripts such as IGF‑1R, MAP3K3, FZD4, NRCAM, SMAD2/3, and HMGB1, thereby modulating critical signaling pathways including AKT, Wnt/β‑catenin, and TGF‑β. Moreover, several studies have implicated miR‐505 in mediating drug response—increasing chemosensitivity in hepatocellular and gastric cancers—and in determining metastatic potential in prostate cancer and glioblastoma."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "23"}]}, {"type": "t", "text": "\n \nBeyond oncogenesis, miR‐505 has been implicated in several non‐neoplastic conditions. In the context of cardiovascular and inflammatory disorders, altered miR‐505 levels contribute to the proinflammatory phenotype observed in familial hypercholesterolemia macrophages and appear as a component of the plasma microRNA signature in hypertension. In neuronal systems, up‐regulation of miR‐505 is linked to enhanced cytotoxicity in a Parkinson’s disease model through repression of NPDC1, while in viral infections such as Borna disease virus 1 the down‐regulation of miR‐505 permits increased autophagy via HMGB1 that favors viral replication. Furthermore, the detection of cell‐free miR‐505 in kidney graft preservation fluid suggests potential utility as a biomarker for predicting delayed graft function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "28"}]}, {"type": "t", "text": "\n \nAdditionally, the regulatory network surrounding miR‐505 is complex and critically influenced by various noncoding RNAs that act as sponges or competing endogenous RNAs. In multiple cancer models, long noncoding RNAs (for example, lncRNA‐CTS in cervical cancer, CRAL in gastric cancer, ZEB1‑AS1 in pancreatic cancer, KTN1‑AS1 in glioblastoma, and PTOV1‑AS1 in hepatocellular carcinoma) as well as circular RNAs (such as circ_0082319 in hepatocellular carcinoma) sequester miR‐505, thereby de‐repressing downstream oncogenes including ZEB2, CYLD, TRIB2, AKT2, PTK2, HMGB1, and RUNX2. Moreover, in neural tumor cells the efficacy of miR‐505 targeting is modulated by competitive interactions with self‐binding motifs in transcripts such as Srsf1. This layered post‐transcriptional regulation underscores the therapeutic potential of restoring or mimicking miR‐505 function, as well as of disrupting its sponging interactions, to inhibit tumor progression and overcome drug resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yusuke Yamamoto, Yusuke Yoshioka, Kaho Minoura, et al. 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