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Functionally, miR‑613 exerts its anti‑tumor effects by targeting a spectrum of oncogenes—such as Notch3, liver X receptor α, sphingosine kinase 2, Daam1, CDK9, E2F5, KRAS, Fzd7, DCLK1, VEGFA, arginase‑2 and AXL—which results in inhibited proliferation, migration, invasion and angiogenesis while promoting cell cycle arrest and apoptosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA complex network of long non‑coding RNAs and circular RNAs modulates the bioactivity of miR‑613 by acting as competing endogenous RNAs (ceRNAs). In several studies, oncogenic lncRNAs such as HOTAIR, LINC00460, LINC00152, UCA1 and others—as well as circRNAs like circCCT3 and circ_0001823—have been shown to “sponge” miR‑613, thereby relieving its inhibition on downstream effectors and facilitating tumor progression. These ceRNA interactions regulate key cellular processes including cell cycle progression, apoptosis, epithelial–mesenchymal transition and metastatic dissemination across multiple tumor types."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical tumor‑suppressive functions, miR‑613 also affects therapeutic responses and metabolic as well as non‑cancerous pathological processes. For instance, in breast cancer, suppression of NAMPT by miR‑613 limits NAD biosynthesis and cell viability, whereas in hepatocellular and esophageal carcinomas, sponging of miR‑613 by MALAT1 or RMRP results in activation of oncogenic pathways. 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