{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNFIC, a member of the Nuclear Factor I family, plays pivotal roles in normal tissue development and differentiation. In mammary epithelial cells, an NF1‐C2 isoform is activated via a non‐canonical nuclear Jak2 pathway by prolactin, thereby regulating milk gene expression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In bone and dental tissues, NFIC acts as a transcriptional switch in bone marrow stromal cells by promoting osteoblast differentiation while inhibiting adipogenesis, regulates osteogenic genes (including IGFBP5), and its alternatively spliced isoforms are critical for proper tooth root formation"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ";"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ";"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ";"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In addition, NFIC is required for chondrocyte proliferation by modulating cell cycle regulators during growth‐plate formation and for pancreatic acinar cell differentiation via interactions with other nuclear receptors"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " NFIC also contributes to the regulation of integrin gene expression in corneal epithelium—impacting cell adhesion and wound healing—as demonstrated for both the α5 and α6 subunit genes"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond these developmental roles, NFIC functions as a versatile transcriptional regulator that modulates chromatin accessibility and works in concert with other factors. It is recruited in cooperation with the glucocorticoid receptor and basic helix–loop–helix proteins to promoter regions—enhancing transcriptional activation of critical genes such as those encoding skeletal muscle sodium channels"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ";"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": " Moreover, global epigenetic studies have implicated NFIC and its NFI‐family cohorts in remodeling chromatin at distal regulatory elements, thereby influencing diverse transcriptional programs."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant regulation of NFIC is increasingly implicated in disease and cancer. In breast cancer, loss of NF1‐C2 (a form of NFIC) is associated with epithelial-to-mesenchymal transition (EMT), increased cellular motility, invasiveness, and ultimately poorer patient survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " In ovarian theca cells from women with polycystic ovary syndrome, diminished NFIC-dependent repression of the CYP17 promoter may underlie augmented androgen biosynthesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": " Additionally, NFIC has been shown to regulate transcription of the aryl hydrocarbon receptor in endometrial cancer"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": "and its altered expression has been observed in gastric cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": " In non-small cell lung cancer, allele-specific NFIC binding to the PD-L1 promoter modulates its inducible expression and affects immunotherapeutic responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " Functional studies in esophageal squamous cell carcinoma indicate that NFIC acts as a tumor suppressor by inhibiting proliferation and metastasis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", while in lung squamous cell carcinoma low NFIC expression correlates with enhanced cell growth and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": " In hematologic malignancies such as acute myeloid leukemia, NFIC supports cell survival, whereas in triple-negative breast cancer overexpression of an NFIC isoform (NFIC1) suppresses EMT by modulating S100A2 and MEK/ERK signaling"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": " Moreover, in colorectal cancer, NFIC acts upstream of CHPF to promote NLRP3 inflammasome activation via MAPK signaling and thereby contributes to tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": " Beyond oncology, NFIC also impacts cardiovascular homeostasis, as its regulation of genes like TSPAN1 and HOPX is linked to ischemic cardiomyopathy, and it participates in cellular senescence through NF1/Smad complexes that modulate oxidative stress responses"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": ";."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jeanette Nilsson, Gunnar Bjursell, Marie Kannius-Janson "}, {"type": "b", "children": [{"type": "t", "text": "Nuclear Jak2 and transcription factor NF1-C2: a novel mechanism of prolactin signaling in mammary epithelial cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cell Biol (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1128/MCB.02095-05"}], "href": "https://doi.org/10.1128/MCB.02095-05"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16847321"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16847321"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Genta Plasari, Alessandra Calabrese, Yves Dusserre, et al. 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