{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNFIB has repeatedly been implicated as a critical fusion partner in the pathogenesis of adenoid cystic carcinoma and related neoplasms. In these tumors, chromosomal translocations fuse NFIB with transcription factors such as MYB or MYBL1, resulting in chimeric transcripts that lead to deregulated MYB pathway activation. Similar rearrangements have been observed not only in typical malignant adenoid cystic carcinoma of the breast, head and neck, and vulva but also in benign tumors such as dermal cylindromas and lipomas, suggesting that NFIB fusion events represent a common mechanism driving neoplastic transformation in secretory gland–derived lesions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in gene fusion–driven tumorigenesis, NFIB functions as a potent regulator of tumor progression in several aggressive cancers. In small cell lung cancer, for example, NFIB is frequently amplified and acts to promote cell viability and metastatic spread. In melanoma, NFIB operates downstream of BRN2 to drive invasion through upregulation of epigenetic regulators, while in triple‐negative breast cancer and other malignancies such as colorectal and gastric cancers, NFIB overexpression fosters proliferation, epithelial–mesenchymal transition, and drug resistance—mediated by effects on key targets like CDKN1A/p21, Snail, HER2 mRNA stability, and even the oxidoreductase ERO1A which augments angiogenesis. Moreover, NFIB levels have been inversely correlated with favorable outcomes in certain contexts, emphasizing its context‐dependent oncogenic potential."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn developmental contexts, NFIB is essential for normal brain formation and cellular differentiation. Haploinsufficiency of NFIB has been linked to intellectual disability, macrocephaly, and abnormal corpus callosum formation, underscoring its role in neurodevelopment. In addition, NFIB contributes to transcriptional regulation in other tissues—for instance, modulating osteoblast function via the control of IGFBP5—and genetic variations in NFIB can influence hepatic expression of cytochrome P450 enzymes, thereby altering drug metabolism (such as clozapine clearance) in patients. Furthermore, in the context of viral infections, NFIB has been implicated in the modulation of host factors that affect HIV-1 replication."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNFIB expression is also subject to regulation by noncoding RNAs, which in turn modulate its function in disease processes. MicroRNAs such as miR‑372/373 and miR‑365 have been shown to target NFIB, affecting hepatitis B virus expression and promoting carcinogenic transformation in cutaneous squamous cell carcinoma. Moreover, in a Parkinson’s disease cell model, alterations in long noncoding RNAs relieve repression of NFIB, thereby influencing neuronal survival and inflammatory responses. Similarly, in avian models of pathogenic Escherichia coli infection, NFIB transcriptionally upregulates immune mediators like RIP2, exacerbating apoptosis and the inflammatory response. These diverse regulatory inputs illustrate the multifaceted role of NFIB as both an effector and a modulated node in cellular signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Marta Persson, Ywonne Andrén, Joachim Mark, et al. 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