{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐381 (miR‐381) has emerged as a critical regulator in cancer biology with context‐dependent, dual functions. In several malignancies—including glioma, lung adenocarcinoma, renal, gastric, colon, cervical, hepatocellular, ovarian, endometrial, breast, rectal cancers and sarcomas—miR‐381 is frequently dysregulated. In many of these tumors, diminished miR‐381 expression has been correlated with aggressive phenotypes, increased proliferation, migration, invasion, epithelial‐to‐mesenchymal transition and chemoresistance; in such cases miR‐381 normally functions as a tumor suppressor by directly targeting oncogenic transcripts such as TMEM16A, LRRC4, PTTG1, MDR1, YY1, FGF7, LRH‐1, ID1, C/EBPα, UBE2C, IGF‐1R, and NASP, thereby modulating key pathways including Wnt/β–catenin, MEK/ERK, PI3K/AKT/mTOR and NF–κB. Conversely, in certain contexts—for example, in a subset of glioblastomas and breast cancers—miR‐381 is overexpressed, where it appears to promote tumor progression by inhibiting tumor suppressor genes. Moreover, emerging studies have demonstrated that external factors such as bisphenol A may reduce miR‐381 levels to indirectly upregulate targets like PTTG1, while aberrant upstream epigenetic regulation by long noncoding RNAs (e.g. SNHG7 and SNHG1) further contributes to its deregulation. Collectively, these findings highlight the potential of miR‐381 both as a circulating diagnostic biomarker and as a therapeutic target for overcoming drug resistance in cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐381 also plays important roles in non‐malignant processes. In models of tissue injury and regeneration, for example, inhibition of miR‐381‐3p has been shown to enhance intestinal epithelial proliferation and barrier function during ischemia/reperfusion injury, while delivery of miR‐381‐3p via small extracellular vesicles promotes chondrogenic differentiation by suppressing TAOK1 and modulating the Hippo pathway. Similarly, in inflammatory and immune‐mediated conditions such as periodontitis, psoriasis and tuberculosis, altered levels of miR‐381‐3p are linked to increased inflammatory cytokine production, monocyte adhesion and impaired antigen presentation. 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