{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐148b has emerged as a key molecular regulator in cancer, where its dysregulated expression contributes to tumorigenesis and progression. In several solid tumors—including gastric, colorectal, pancreatic, hepatocellular, non–small cell lung, cervical, breast, oral, and bladder cancers—miR‐148b is frequently downregulated, and its restoration elicits tumor‐suppressive effects. Mechanistically, miR‐148b targets critical oncogenic effectors such as DNA methyltransferase 1 (DNMT1), AMPKα1, WNT1, the cholecystokinin‐2 receptor (CCK2R), p55PIK, solute carrier family 2 member 1 (SLC2A1/GLUT1), and MAP3K9, as well as signaling mediators involved in integrin and proteasome pathways. In addition, its interplay with other microRNAs, for example the antagonism with miR‐214, further refines its ability to modulate proliferation, apoptosis, invasion, metastasis, and even treatment response—including enhanced chemosensitivity and radiosensitivity—in these malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond malignancy, miR‐148b also plays important roles in non‐neoplastic conditions. In IgA nephropathy, for instance, miR‐148b is upregulated in immune cells and renal tissues, where it suppresses enzymes such as C1GALT1—and in some studies megalin—thereby contributing to the aberrant O‐glycosylation of IgA1. Altered circulating levels of miR‐148b have been reported in other disorders as well; its modulation has been linked to changes in radiosensitivity in non–Hodgkin’s lymphoma, endothelial dysfunction under hypoxic stress (via interactions with lncRNA H19), and even reduced insulin sensitivity during the early transition to physical inactivity. Furthermore, measurements of serum miR‐148b have shown diagnostic promise in conditions such as ischemic stroke and may reflect immune response alterations observed in childhood atopic asthma."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the cumulative evidence indicates that miR‐148b functions as a central molecular switch—modulating cellular proliferation, apoptosis, invasion, metabolism, and differentiation in a context‐dependent manner. Whether by suppressing oncogenic signaling in tumors, dictating aberrant immune glycosylation in kidney disease, or influencing cellular stress and therapeutic responsiveness, miR‐148b holds promise as both a diagnostic biomarker and a therapeutic target. Its integration into regulatory networks involving long noncoding RNAs and other microRNAs further emphasizes its multifaceted role in orchestrating disease processes and treatment outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yong-Xi Song, Zhen-Yu Yue, Zhen-Ning Wang, et al. 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