{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNR4A1—also known as Nur77 or TR3—is a multifaceted orphan nuclear receptor whose activity governs critical cell‐intrinsic decisions in cancer. In several tumor models (including lung, colon, pancreatic and breast cancers), NR4A1 exhibits dual functions: its nuclear activity promotes gene transcription that can enhance cell proliferation and survival, whereas its stimulus‐dependent export to the mitochondria enables it to interact with proteins such as Bcl‐2 or p53, thereby triggering apoptotic or other programmed cell death pathways. This switch in function—with effects ranging from the conversion of anti‐apoptotic molecules into pro‐death factors to the modulation of stress responses—underscores the potential of NR4A1 as a therapeutic target in diverse malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its cell‐autonomous roles in tumor cells, NR4A1 is rapidly induced by antigen‐receptor and inflammatory signals in leukocytes and vascular cells. In T and B lymphocytes NR4A1 serves as a highly specific immediate‐early marker of receptor activation and is implicated in the program of T cell hyporesponsiveness or “exhaustion” observed in solid tumors. Similarly, in innate immune and vascular contexts, NR4A1 participates in the negative regulation of pro‐inflammatory cascades and modulates angiogenic and DNA damage responses—functions that may ultimately influence the outcome of immune–inflammatory diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cell fate and immunity, NR4A1 orchestrates key metabolic and stress‐response pathways. It regulates steroidogenic gene expression in endocrine tissues, interferes with energy‐sensing networks—for example by sequestering LKB1 and modulating AMPK activity—and adjusts the balance between glycolysis and gluconeogenesis in hepatocellular carcinoma. 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