{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe miR‐302/367 cluster – with miR‐367 as a key member – is critically involved in maintaining pluripotency and regulating cell cycle progression in embryonic stem cells, and its ectopic expression can reprogram somatic cells. In this context, several studies have demonstrated that miR‐367 participates in both promoting and modulating stem‐like properties, while its detection in biological fluids offers promising diagnostic potential. For example, its high expression in stem cells has been linked to enhanced reprogramming efficiency and altered apoptotic pathways (see."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": " Moreover, the detection of elevated circulating miR‐367 levels has been successfully used to distinguish germ cell tumors with high sensitivity, and its synergistic role in enhancing reprogramming‐based tumor suppression has also been reported."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various cancer types the expression and function of miR‐367 exhibit a context‐dependent duality. In malignancies such as non–small cell lung cancer, uveal melanoma, medulloblastoma, and esophageal as well as germ cell tumors, elevated miR‐367 levels have been linked to increased proliferation, invasion, and stem‐like traits. Mechanistically, this oncogenic influence is mediated by direct targeting of tumor suppressors – for instance, regulating RYR3 in breast cancer, FBXW7 and PTEN in lung and uveal melanoma, as well as modulating downstream effectors (e.g. Let‐7, SUZ12) in several tumor models."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "30"}]}, {"type": "t", "text": " In contrast, in cancers such as cervical and prostate tumors, lower levels of miR‐367‐3p have been observed; restoration of its expression in these settings suppresses proliferation and invasion through targeting molecules like SPAG5 and Rab23"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "27"}]}, {"type": "t", "text": ", underscoring a cell‐type–specific role for this microRNA.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its effects on tumor cell intrinsic pathways, miR‐367 has been implicated in modulating treatment responses and the tissue microenvironment. Its expression correlates with paclitaxel sensitivity in ovarian cancer cells, and by influencing signaling pathways such as Wnt/β‐catenin and Let‐7, it contributes to the maintenance of cancer stem cell properties in lung tumors."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": " Furthermore, emerging evidence indicates that miR‐367 can regulate non–tumor cell functions – for example, by modulating microglia polarization via targeting CEBPA in intracerebral hemorrhage and by exhibiting altered expression in cardiac fibrosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": " Finally, studies in prostate and breast cancers suggest that the circulating levels of miR‐367 may serve as valuable biomarkers for disease stratification."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "M Fareh, L Turchi, V Virolle, et al. 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