{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑328 is emerging as a versatile regulator in human disease, particularly in cancer, where it can act either as a tumor suppressor or as an oncomiR depending on the cellular context. In chronic myelogenous leukemia, loss of miR‑328 disrupts differentiation by interfering with RNA‑binding protein decoy functions, while its restoration promotes blast differentiation and limits cell survival. In hepatocellular carcinoma, miR‑328‑5p promotes malignant behaviors through repression of the tumor‐suppressive gene DAB2IP. Similarly, in non‑small cell lung cancer, elevated miR‑328 enhances cell migratory potential and predisposes tumors to brain metastasis by modulating PRKCA activity. Other studies in osteosarcoma and glioma have demonstrated that upregulation or ectopic expression of miR‑328 can inhibit matrix metalloproteinase‑2 or modulate Wnt signaling via targeting SFRP1, thereby reducing invasion and proliferation. In several solid tumors—including breast, gastrointestinal, colon, esophageal, cervical, and gastric cancers—miR‑328 controls key mediators such as CD44, COL1A1, CPT1A, and other signaling effectors, underscoring its context‐dependent dual roles in promoting or inhibiting tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, miR‑328 exerts its functions through direct targeting of key mRNAs as well as by acting as a decoy for regulatory proteins. For example, it directly downregulates ABCG2, thereby influencing drug efflux and chemoresistance, and enhances radiosensitivity by targeting gamma‑H2AX. In pancreatic cancer, miR‑328 targets ADAM8 to inhibit tumor growth and metastasis, whereas in epithelial cancers it reduces PTPRJ levels, thus promoting proliferation. Its activity is further modulated by noncoding RNAs; specific long noncoding RNAs and circular RNAs act as sponges for miR‑328 to control the expression of downstream effectors such as SRCIN1 and NOTCH3. Moreover, miR‑328 modulates the activity of transporter proteins—for instance, exosomal miR‑328 derived from intestinal cells correlates with reduced BCRP function—and influences metastatic potential by targeting CD44 in early gastric cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its mechanistic roles in cancer biology, miR‑328 is gaining attention as a promising diagnostic and prognostic biomarker in a range of clinical settings. Altered circulating levels of miR‑328 have been documented in cardiovascular diseases such as acute myocardial infarction and atrial fibrillation, as well as in traumatic brain injury, where its upregulation correlates with injury severity. Furthermore, changes in miR‑328 expression have been associated with treatment response in acute myeloid leukemia and even linked to retinal disorders like high myopia by virtue of SNPs in its binding sites. In vascular biology, miR‑328 contributes to endothelial cell protection in atherosclerosis by targeting FOXO4. Additional studies in indeterminate thyroid lesions and atrial tissue further support its potential translational utility in non‑cancer pathologies and neurobiology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Anna M Eiring, Jason G Harb, Paolo Neviani, et al. 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