{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑744 has emerged as a multifunctional regulator in a variety of cancers, exhibiting context‐dependent roles that can be either oncogenic or tumor suppressive. In pancreatic and prostate cancers, its upregulation potentiates oncogenic signalling—by activating the Wnt/β‑catenin pathway through direct targeting of negative regulators such as secreted frizzled‑related protein 1, glycogen synthase kinase‑3β and transducin‑like enhancer of split—as well as promoting metastasis via modulation of transcription factors like c‑FOS. In nasopharyngeal and head and neck carcinomas, elevated miR‑744 levels are associated with enhanced migration and invasion through transcriptional regulation of pro‑tumorigenic genes (e.g. ARHGAP5 and MMP‑9). Conversely, in other tumour types such as epithelial ovarian, papillary thyroid and certain colorectal cancers, enforced expression of miR‑744–5p restricts cell proliferation and induces apoptosis by targeting key oncogenic mediators including Bcl‑2, c‑myc and ARF1. Moreover, in osteosarcoma, aberrant miR‑744 expression promotes proliferation via the PTEN/AKT pathway, while in a subset of colorectal tumours it contributes to chemoresistance by suppressing BIN1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct effects on tumour cell behaviour, miR‑744–5p is subject to intricate regulation by various non‑protein‐coding RNAs that function as competing endogenous RNAs. In lung adenocarcinoma, the oncogenic long non‑coding RNA MAFG‑AS1 acts as a molecular sponge for miR‑744–5p, thereby relieving repression of nearby transcription factors. Similar competitive interactions have been described in glioma and pituitary adenoma, where lncRNA LINC01116 sequesters miR‑744–5p to preserve the expression of oncogenic targets such as MDM2 and HOXB8. Furthermore, in colorectal and ovarian cancers, deregulated lncRNAs like MNX1‑AS1 contribute to malignant progression by competitively binding miR‑744–5p, a process that is reinforced by the delivery of miR‑744–5p via mesenchymal stem cell‑derived extracellular vesicles."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its cell‐intrinsic effects in cancer, miR‑744 plays pivotal roles as a biomarker and modulator of non‑malignant pathophysiological processes. Its altered expression in circulating exosomes has been linked to hepatocellular carcinoma progression and chemoresistance, while downregulation in cardiac fibroblasts alleviates angiotensin II–induced collagen deposition and fibrogenesis through direct targeting of transforming growth factor‑β1. In renal mesangial cells, miR‑744 enhances type I interferon signalling by repressing negative phosphatases, and in psoriasis it not only promotes keratinocyte proliferation but also delays differentiation via inhibition of targets such as KLLN. Moreover, miR‑744–5p has shown promise as a biodosimeter for radiation exposure, and its progressive upregulation during T cell activation suggests an important role in modulating T cell differentiation and functionality through targeting regulators like STK11."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yuan Fang, Xiaoxia Zhu, Jian Wang, et al. 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