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Mechanistically, MIR153‐2 directly targets key pro‐tumorigenic regulators including SNAI1, ZEB2, Snail, ADAM19, IGF1R, MCL1 and others, thereby curbing oncogenic signaling pathways (e.g. Raf/MEK, PI3K/AKT, and Wnt/β‐catenin) and, in cases such as pancreatic cancer, enhancing sensitivity to chemotherapeutic agents like gemcitabine."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its intrinsic tumor‐suppressive capacity, MIR153‐2 is tightly regulated by an array of noncoding RNAs. Several long noncoding RNAs and circular RNAs act as competing endogenous RNAs that “sponge” MIR153‐2, thereby indirectly de‐repressing oncogenic targets. In contexts such as non‐small‐cell lung cancer and esophageal squamous cell carcinoma, manipulation of MIR153‐2 levels has been shown to modulate drug sensitivity (to agents including gefitinib and cisplatin). Moreover, in neurodegenerative and neurological settings, MIR153‐2 regulates proteins like α‐synuclein in Parkinson’s disease and modulates HIF‐1α expression in epilepsy, illustrating its broader regulatory influence beyond oncogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition, MIR153‐2 influences other critical cellular processes. For instance, in dental pulp stem cells, miR‐153‐3p (a form of MIR153‐2) negatively regulates osteogenic differentiation by directly targeting core‐binding factor β, suggesting a role in bone regeneration. 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