{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNAC1 (nucleus accumbens‐associated protein 1), a member of the BTB/POZ family of transcriptional regulators, is frequently overexpressed in a variety of human carcinomas—including ovarian, cervical, endometrial, and others—where it exerts potent oncogenic functions. Elevated NAC1 levels have been shown to promote tumor cell proliferation, survival, migration, and resistance to chemotherapeutic agents by repressing tumor suppressor pathways (for example, via down‐regulation of Gadd45GIP1 and modulation of the Gadd45 signaling cascade) and by fostering a chemoresistant phenotype. In ovarian serous carcinomas and cervical cancers, high NAC1 expression and gene amplification correlate with early tumor recurrence and poor clinical outcome, underscoring its role as a key driver of malignant progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, NAC1 functions through several interrelated processes. It forms discrete nuclear bodies via homooligomerization mediated by its BTB/POZ domain, and its activity is fine‑tuned by post‑translational modifications such as SUMOylation. Through these interactions, NAC1 not only acts as a corepressor for other POZ/BTZ proteins but also regulates the transcription of key downstream targets—such as FOXQ1 and HOXA9—that modulate epithelial–mesenchymal transition and cell motility. Moreover, noncoding RNAs (for example, LINC00319 and FOXP4‑AS1) and microRNAs (including miR‑339‑5p and miR‑760) have been identified as upstream regulators that control NAC1 expression, further highlighting its integration into complex regulatory networks that influence tumor metabolism, senescence (via ΔNp63/p21 modulation), and the formation of higher‑order transcriptional complexes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its well‐established oncogenic roles, NAC1 is emerging as a multifunctional protein with broader biological implications. A recurrent de novo mutation in NACC1 has been implicated in a neurodevelopmental disorder marked by intellectual disability and other neurological deficits, underscoring its importance in normal central nervous system function. Furthermore, recent studies indicate that NAC1 can bridge components of the innate immune system by facilitating the interaction between MAVS and TBK1 to promote type I interferon responses. Tissue‑specific differences are also evident—for instance, in pancreatic ductal adenocarcinoma, low NAC1 expression correlates with poor prognosis, while in hepatocellular carcinoma, NAC1 promotes tumor progression and chemoresistance, partly through regulation by miR‑760. Collectively, these diverse functions not only reveal NAC1’s central role in tumorigenesis and therapy resistance but also nominate it as a promising target for novel therapeutic strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kentaro Nakayama, Naomi Nakayama, Ben Davidson, et al. 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