ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Autophagy Deficiency Induced by SAT1 Potentiates Tumor Progression in Triple-Negative Breast Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Emerging roles of RNA N5-methylcytosine modification in reproductive physiology and gynecological diseases.Epigenetics · 2026Review
- A biomarker-driven approach to targeting polyamine depletion in triple negative breast cancer.Biomarker research · 2026Article
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- USP18 promotes clear cell renal cell carcinoma progression by regulating the ubiquitination and stability of YBX3.iScience · 2026Article
- 5-Methylcytidine RNA Epitranscriptomics in Women's Health and Disease: Mechanisms and Clinical Implications.Cells · 2026Review
- Bioinformatics Analysis of Ferroptosis-Related Driver Genes in Stanford Type A Aortic Dissection.Current issues in molecular biology · 2026Article
- Regulation of mitochondrial ROS by C15ORF48 in a basal cell subpopulation contributes to chemotherapy resistance in TNBC.Science advances · 2026Article
- PTPN1 Regulation via YBX1-PTBP1 Interaction Promotes Fibroblast Activation and Fibrotic Remodeling in the Lung.International journal of biological sciences · 2026Article
- A Novel Autophagy InhibitorResearch (Washington, D.C.) · 2026Article
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- ZDHHC9 and spermine metabolism: a palmitoylation-driven pathway to prostate carcinogenesis.Journal of translational medicine · 2025Article
- The Cx43-Mediated Autophagy Mechanism Influences Triple-Negative Breast Cancer Through the Regulation of Rab31.Cancers · 2025Article
- RNA m5C methylation in cancer: mechanisms and biological impact.Oncogenesis · 2025Review
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- Overexpression of alcohol dehydrogenase 1 A inhibits the progress of triple negative breast cancer via Wnt/β-catenin signaling.Scientific reports · 2025Article
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- The functions and regulation of transcription factor YBX1 in cancers.Molecular biology reports · 2025Review
- Dauricine Overcomes Osimertinib Resistance in Lung Cancer by Inducing Ferroptosis via Stabilizing SAT1.Cancer science · 2025Article
- m5C RNA methylation in cancer: from biological mechanism to clinical perspectives.European journal of medical research · 2025Review
- Reduction of NFX1-123 and HPV 16 E6 and E7 Decreased Telomerase and CENP-F in Cervical Cancer Cell Lines.Cancers · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Aggressive triple-negative breast cancer (TNBC) still lacks approved targeted therapies, requiring more exploration of its underlying mechanisms. Previous studies have suggested a potential role of SAT1 (Spermidine/Spermine N1-acetyltransferase 1) in cancer, which needs to be further elucidated in breast cancer. In this study, highly expressed SAT1 in TNBC signified worse patient prognoses. And SAT1 knockdown effectively inhibited the proliferation and migration abilities of TNBC cells in vitro and in vivo. In terms of mechanism, the transcription factor JUN enhanced SAT1 transcriptional activity by binding to its promoter region. Then, SAT1 protein in the cytoplasm engaged in directly binding with YBX1 for sustaining YBX1 protein stability via deubiquitylation mediated by the E3 ligase HERC5. Further, SAT1 was found to suppress autophagy remarkably via stabilization of mTOR mRNA with the accumulation of YBX1-mediated methyl-5-cytosine (m5C) modification. These findings proved that SAT1 drives TNBC progression through the SAT1/YBX1/mTOR axis, which may provide a potential candidate for targeted therapy in advanced TNBC.
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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 OpenQuestion graph.