{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐372 has emerged as a pivotal regulator in early developmental and stem cell contexts. In human embryonic stem cells it is a key component of the ESCC (embryonic stem cell‐specific cell cycle) microRNA family that promotes somatic cell reprogramming by accelerating the mesenchymal–epithelial transition and by repressing multiple downstream regulators. Elevated levels of miR‐372 (and its cluster mates) are also detectable in the serum of patients with germ cell tumors, where they serve as highly sensitive biomarkers, and in germline differentiation where they promote primordial germ cell–like cell formation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn diverse cancers, however, miR‐372 exhibits context‐dependent functions. In some tumors—such as testicular germ cell tumors, certain gliomas, and colorectal, hepatocellular, lung squamous cell, and parathyroid carcinomas—upregulation of miR‐372 is associated with oncogenic activities; it can promote proliferation, invasion, and migration by impairing cell cycle checkpoints and by modulating key regulators (for example, LATS2, CDK2, cyclin A1, and NF‐κB signaling components). In contrast, in other malignancies including cervical, endometrial, pancreatic, and prostate cancers, miR‐372 appears to function as a tumor suppressor by inducing cell cycle arrest and apoptosis. Moreover, its dysregulated expression has been linked to poor prognostic features in several tumors, and in some settings (such as in renal cell carcinoma) its precise role remains to be fully elucidated."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "26"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cell fate determination and tumor cell proliferation, miR‐372 is also a key modulator of cellular stress responses, including autophagy, antiviral signaling, and chemoresistance. Functional studies have revealed that miR‐372 directly targets crucial mediators of the autophagic process (such as SQSTM1, ULK1, ATG5, and ATG12), thereby affecting the response to nutrient stress, radiotherapy, and chemotherapy. In addition, by modulating mitochondrial dynamics and metabolic flux, miR‐372 contributes to the termination of type I interferon and inflammatory cytokine production during late viral infections. Finally, interactions with long non‐coding RNAs in competing endogenous RNA networks further fine‐tune its activity in processes such as epithelial–mesenchymal transition and drug resistance, while emerging genetic variants may influence individual susceptibility to virus‐related pathogenesis and other conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "37"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Deepa Subramanyam, Samy Lamouille, Robert L Judson, et al. 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