ArticleNature communications2025
A noncanonical role of SAT1 enables anchorage independence and peritoneal metastasis in ovarian cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Glutamine-driven metabolic reprogramming promotes CAR-T cell function through mTOR-SREBP2 mediated HMGCS1 upregulation in ovarian cancer.Journal of translational medicine · 2025Trial
- Article
- Bioinformatics Analysis of Ferroptosis-Related Driver Genes in Stanford Type A Aortic Dissection.Current issues in molecular biology · 2026Article
- Role of solute carrier family 7 member 7 in cancer: opportunities for tumor microenvironment research.Journal for immunotherapy of cancer · 2026Review
- ZDHHC9 and spermine metabolism: a palmitoylation-driven pathway to prostate carcinogenesis.Journal of translational medicine · 2025Article
- Metabolic support protects mucosa from ferroptosis in radiation-induced mucositis.Nature communications · 2025Article
- Lactate Enhances Non-Homologous End Joining Repair and Chemoresistance Through Facilitating XRCC4-LIG4 Complex Assembly in Ovarian Cancer.Biomedicines · 2025Article
- Regulation of polyamine interconversion enzymes affects α-Synuclein levels and toxicity in a Drosophila model of Parkinson's Disease.NPJ Parkinson's disease · 2025Article
- SAT1 promotes the progression of OA by regulating TRIM33-mediated p53 acetylation to enhance ferroptosis.PloS one · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Anchorage-independent survival of ovarian tumor cells in ascites is the initial and critical step for peritoneal metastasis. How ovarian tumor cells achieve anchorage independence remains unclear. Here we show that a noncanonical role of spermidine/spermine N1-acetyltransferase 1 (SAT1) dictates anchorage-independent cell survival and potentiates metastatic dissemination in ovarian cancer. SAT1-high cancer cells are prevalent in ascitic tumors, and high SAT1 expression in primary tumors is linked to increased peritoneal metastasis rates in ovarian cancer patients. Mechanistically, SAT1 noncanonically acetylates H3K27 domains in multiple mitosis-regulating genes, increasing their transcriptional levels and protecting disseminating cells from aberrant mitosis and mitotic cell death. Notably, the acetylation of H3K27 by SAT1 depends on the reductive carboxylation of glutamine to supply acetyl-CoA in the nucleus. SAT1 inhibition with the small-molecule inhibitor ginkgolide B attenuates the metastatic tumor burden in mouse models. We conclude that SAT1 inhibition is a promising therapeutic strategy for metastatic ovarian cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.