{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐31 is a multifunctional regulator whose activity in cancer is strikingly context dependent. In several epithelial malignancies such as lung, head and neck, oral squamous, colorectal, gastric and even hematologic cancers, over‐expression of miR‐31 has been shown to promote tumorigenesis through direct targeting of tumor‐suppressive genes (for example, LATS2, PPP2R2A, FIH‐1, RASA1, and SATB2) and by modulating key pathways including RAS/MAPK, NF‐κB, and HIF signaling. In lung and head and neck cancers, miR‐31 upregulation enhances cell proliferation and tumor growth, whereas in colorectal cancers its aberrant expression is linked to aggressive behavior and poor prognosis. In contrast, in breast, prostate and certain other cancers, miR‐31 is down‐regulated and acts as a metastasis suppressor by inhibiting pro‐metastatic genes such as RhoA, WAVE3, E2F6, and PKCε. Furthermore, genomic losses, epigenetic silencing, and noncoding RNA–mediated sponging events further influence its levels and functions, underscoring miR‐31’s complex oncogenic and tumor‐suppressive roles."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "26"}]}, {"type": "t", "text": "\n \n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in malignant cells, miR‐31 also orchestrates a variety of non–tumor cell processes. In the immune system, it modulates T‐cell responses by directly repressing FOXP3 in regulatory T cells, thereby influencing immune tolerance, and its altered expression has been associated with defects in cytokine signaling in conditions such as systemic lupus erythematosus. In vascular and inflammatory contexts, miR‐31 is induced by inflammatory cytokines in endothelial cells to negatively regulate adhesion molecule expression and in keratinocytes it promotes wound healing by enhancing proliferation and migration via targets like EMP1. In Duchenne muscular dystrophy, miR‐31 represses dystrophin expression, and its inhibition can partially rescue dystrophin levels."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "6"}, {"type": "fg_fs", "start_ref": "27", "end_ref": "31"}]}, {"type": "t", "text": "\n \n"}, {"type": "p", "children": [{"type": "t", "text": "\nmiR‐31 further regulates stem cell differentiation, angiogenesis, and vascular biology. In mesenchymal stem cells, down‐regulation of miR‐31 promotes osteogenic differentiation by releasing inhibition of bone‐specific transcription factors such as Osterix and by modulating components of the Wnt/Frizzled pathway, contributing to age‐related deficits in bone formation. Moreover, miR‐31 carried in microvesicles from adipose‐derived stem cells enhances angiogenic responses by targeting antiangiogenic regulators, while in vascular smooth muscle cells its elevated expression promotes proliferation through inhibition of LATS2. In addition, miR‐31 plays a pivotal role in vascular lineage decisions by repressing transcription factors like PROX1 to influence lymphatic versus blood vessel development. Noncoding RNAs, including circular and long noncoding RNAs, further refine miR‐31 availability and activity in these settings, adding an additional layer to its multifaceted regulatory network."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "32", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xi Liu, Lorenzo F Sempere, Haoxu Ouyang, et al. 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