{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐23b has emerged as a versatile regulator in cancer biology where its impact is highly context‐dependent. In breast cancer, for example, exosomal transfer of miR‐23b from bone marrow mesenchymal stem cells promotes cellular dormancy by suppressing targets such as MARCKS, while in cervical cancer its downregulation—partly driven by HPV oncoprotein‐mediated p53 inactivation—leads to upregulation of prometastatic factors like urokinase‐type plasminogen activator. In prostate, bladder, renal, glioma, gastric, ovarian, and multiple myeloma cells, miR‐23b modulates key processes including proliferation, invasion, epithelial–mesenchymal transition, and chemoresistance by targeting diverse effectors such as Src kinase, VHL, proline oxidase, Notch2, Zeb1, and RUNX2. These studies collectively indicate that miR‐23b can function either as a tumor suppressor or as an oncogenic facilitator depending on the cellular state and microenvironment."}, {"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": "\nBeyond its role in tumor progression, miR‐23b is a critical modulator of cellular responses that underlie chemoresistance, metabolism, and cell fate. Its repression by oncogenic signals such as c‐Myc is associated with enhanced glutamine catabolism, whereas its enforced expression can reverse multidrug resistance by targeting autophagy regulators like ATG12 and HMGB2. In models of diabetic nephropathy, miR‐23b attenuates epithelial–mesenchymal transition by directly inhibiting HMGA2, and in traumatic brain injury its overexpression limits autophagy‐mediated neuronal loss. Moreover, miR‐23b has been implicated in the regulation of osteogenic differentiation of mesenchymal stem cells via direct suppression of runx2, with circulating levels serving as potential biomarkers in osteoporosis and related pathologies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its oncogenic and metabolic roles, miR‐23b contributes to the regulation of normal physiological processes and may serve as a valuable biomarker in non‐malignant diseases. It participates in endothelial responses to mechanical forces, thereby modulating cell cycle arrest under shear stress conditions, and its dysregulated expression has been linked to atrial fibrosis through direct targeting of TGF‐β receptor components. 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