ArticleInternational journal of molecular sciences2025
NAC1 Regulates PCK2 Expression and Activates Truncated Gluconeogenesis for Growth Advantage in Ovarian Cancer Cells.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Lipid metabolic reprogramming in ovarian cancer: molecular mechanisms and therapeutic implications.Medical molecular morphology · 2026Review
- Determinants of skeletal muscle loss during initial treatment in patients with ovarian cancer: a brief report.Frontiers in oncology · 2026Article
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Authors and funding
5 authors.
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Abstract
Nucleus accumbens-associated protein 1 (NAC1), a cancer-related transcriptional regulator, is overexpressed in several malignancies, including ovarian cancer. However, its role in ovarian carcinogenesis remains unclear. We aimed to investigate whether NAC1 contributes to metabolic adaptation in endometriosis-related ovarian neoplasms (ERONs) and elucidate its regulatory mechanisms. The clinical relationship between NAC1 and its potential downstream target, phosphoenolpyruvate carboxykinase isoform 2 (PCK2), was examined using immunohistochemical analysis of ovarian cancer specimens. A cell viability assay was performed to clarify the impact of PCK2 on ovarian cancer cell viability. Reporter and chromatin immunoprecipitation (ChIP) assays were conducted to evaluate transcriptional regulation by NAC1. Metabolomic profiling was performed to assess the functional impact of the NAC1-PCK2 axis. A positive correlation between NAC1 and PCK2 expression was observed, and co-expression was associated with poor long-term survival. Knockdown of PCK2 led to a significant reduction in cell viability, indicating that PCK2 is required for maintaining cell survival. Reporter and ChIP assays confirmed that NAC1 directly binds to the PCK2 promoter via the CATG motif. The metabolomic analysis demonstrated that NAC1 promotes truncated gluconeogenesis and de novo serine synthesis through PCK2 upregulation. These findings suggest that NAC1 contributes to ovarian cancer progression by promoting metabolic adaptation, highlighting the NAC1-PCK2 axis as a potential therapeutic target for ERONs.
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