{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐574 (miR‐574) comprises two major, functionally distinct strands—miR‐574‐5p and miR‐574‐3p—that are emerging as versatile biomarkers and diagnostic tools in a wide range of human disorders. Several studies have reported aberrant levels of these miRNAs in biological fluids and exosomes derived from tumor cells. For example, serum‐based miRNA profiling in non–small‐cell lung cancer patients and the isolation of miRNAs from glioblastoma microvesicles underscore the potential of miR‐574 as a minimally invasive indicator for early detection of cancer and other diseases such as esophageal squamous cell carcinoma, hepatocellular carcinoma, coronary artery disease, and prostate cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, miR‐574 displays context‐dependent functions in oncogenesis and tumor progression. In certain cancers such as papillary thyroid carcinoma, miR‐574‐5p acts by targeting key suppressors (for example, suppressor of cancer cell invasion) thereby modulating the Wnt/β‐catenin pathway and promoting proliferation and migration. In non–small‐cell and small‐cell lung cancers, upregulation of miR‐574‐5p has been linked to enhanced cell motility through repression of protein tyrosine phosphatases and consequent β‐catenin tyrosine phosphorylation. In gastric cancer, the miR‐574‐3p arm appears to exert tumor‐suppressive effects by inhibiting epithelial–mesenchymal transition via direct targeting of transcription factors such as ZEB1, which in turn improves cisplatin sensitivity. Moreover, studies in triple‐negative breast cancer, thyroid cancer, colorectal cancer, and in the regulation of drug metabolizing enzymes (e.g. CBR1) indicate that miR‐574 functions as part of intricate regulatory networks that include interactions with long noncoding RNAs and single‐nucleotide polymorphisms. Together, these findings demonstrate that miR‐574 orchestrates key processes—from cell cycle control to chemoresistance—thereby serving both oncogenic and tumor‐suppressive roles depending on the cellular context."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, miR‐574 is also implicated in diverse non–neoplastic processes. In mesenchymal stem cell differentiation, miR‐574‐3p is rapidly induced by the master chondrogenic transcription factor Sox9 to modulate targets such as retinoid X receptor α, suggesting a role in cartilage and bone lineage commitment. Altered miR‐574 expression is furthermore associated with white adipose tissue hypertrophy and impaired metabolic homeostasis, as seen in gestational diabetes. In addition, aberrant miR‐574 levels contribute to cardiac fibrosis by promoting fibroblast‐to‐myofibroblast conversion, to acute lung injury by attenuating endoplasmic reticulum stress through complement regulation, and to rheumatoid arthritis by enhancing osteoclast differentiation via Toll‐like receptor 7/8 activation. Finally, ectopic expression studies during hepatic differentiation underscore its participation in lineage specification from umbilical cord–derived mesenchymal stem cells. These findings highlight miR‐574 as a multifunctional regulator in both homeostatic and stress‐induced contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kristen M Foss, Chao Sima, Donatella Ugolini, et al. 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