{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑498 is a multifunctional non‑coding RNA that plays context‑dependent roles in human malignancies. In several solid tumors its downregulation is associated with tumor suppression. For example, in ovarian cancer, vitamin D induces miR‑498 expression, which in turn downregulates human telomerase reverse transcriptase (hTERT) mRNA, thereby hindering cell proliferation and tumor growth. Similarly, in colorectal adenocarcinoma, low miR‑498 levels are linked to enhanced proliferation, and restoration of its expression enforces cell cycle arrest. In retinoblastoma and esophageal squamous cell carcinoma, miR‑498 overexpression triggers apoptosis and disrupts oncogenic signaling, while in liver malignancies—including studies in hepatocellular carcinoma—miR‑498 suppresses migration and invasion by targeting factors such as ZEB2."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn other contexts, however, miR‑498 exhibits oncogenic properties. In triple‑negative breast cancer, for instance, miR‑498 is overexpressed and directly targets key tumor suppressors—including BRCA1 and PTEN—thereby promoting proliferation and migration. A similar pro‑tumorigenic role has been observed in prostate cancer, where forced miR‑498 expression enhances invasion and diminishes apoptosis via modulation of epithelial–mesenchymal transition and AKT signaling. In contrast, in non‑small cell lung cancer and acute myeloid leukemia, re‑establishing miR‑498 levels improves sensitivity to targeted therapies and radiation by inhibiting components of the PI3K/AKT pathway and downregulating immunomodulatory molecules such as TIM‑3."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, the activity of miR‑498 is intricately modulated by upstream non‑coding RNAs that act as competing endogenous RNAs. In virus‑associated cancers, miR‑498 directly targets the 3′‑UTR of the KSHV lytic switch protein RTA, thereby controlling viral reactivation. In several tumors, oncogenic circular RNAs and long non‑coding RNAs sequester miR‑498—thereby relieving its inhibitory effects on downstream targets. For example, in lung cancer, circFADS2 binds miR‑498 to promote oncogenic progression, while in glioma, lncRNA CASC11 functions as a molecular sponge that impairs miR‑498‑mediated repression of FOXK1. In inflammatory chondrocytes, circRNA modulation of miR‑498 controls mTOR expression and influences extracellular matrix degradation. Similar ceRNA networks have been identified in esophageal carcinoma (via lncRNA TUG1 regulating CDC42), in clear cell renal cell carcinoma (through hsa_circ_0085576 affecting YAP1), in osteosarcoma (via circ_0032463 altering LEF1 levels), and in endometrial and cervical cancers where lncRNAs such as HOXB‑AS3 and MIR9‑3HG modulate miR‑498 availability to impact EP300 and ADAM9 expression. Additionally, in malignant melanoma and colorectal cancer, miR‑498 exerts tumor‑suppressive effects by directly targeting UBE2T and ATP5E, respectively, with its loss correlating with poorer outcomes. Other reports further implicate miR‑498 in enhancing radiosensitivity by inhibiting DNMT3b and in modulating cell death pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ravi Kasiappan, Zheng Shen, Anfernee K-W Tse, et al. 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