ArticleCell death and differentiation2014
Suppression of acetylpolyamine oxidase by selected AP-1 members regulates DNp73 abundance: mechanistic insights for overcoming DNp73-mediated resistance to chemotherapeutic drugs.
Article in Cell death and differentiation, 2014. 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, 34 citations in OpenAlex.
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- Unravelling molecular mechanism of oral squamous cell carcinoma and genetic landscape: an insight into disease complexity, available therapies, and future considerations.Frontiers in immunology · 2025Review
- Two-polarized roles of transcription factor FOSB in lung cancer progression and prognosis: dependent on p53 status.Journal of experimental & clinical cancer research : CR · 2024Article
- Polyamine Catabolism Revisited: Acetylpolyamine Oxidase Plays a Minor Role due to Low Expression.Cells · 2024Article
- Enzymatic-related network of catalysis, polyamine, and tumors for acetylpolyamine oxidase: from calculation to experiment.Chemical science · 2024Article
- Comprehensive analysis of a novel RNA modifications-related model in the prognostic characterization, immune landscape and drug therapy of bladder cancer.Frontiers in genetics · 2023Article
- Polyamine Oxidase Expression Is Downregulated by 17β-Estradiol via Estrogen Receptor 2 in Human MCF-7 Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.Molecular biology · 2022Article
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- Inflammatory Mediators in Oral Cancer: Pathogenic Mechanisms and Diagnostic Potential.Frontiers in oral health · 2021Review
- Cellular and Animal Model Studies on the Growth Inhibitory Effects of Polyamine Analogues on Breast Cancer.Medical sciences (Basel, Switzerland) · 2018Review
- The elevated activation of NFκB and AP-1 is correlated with differential regulation of Bcl-2 and associated with oral squamous cell carcinoma progression and resistance.Clinical oral investigations · 2017Article
- Ultraconserved long non-coding RNA uc.63 in breast cancer.Oncotarget · 2017Article
- SMYD2 lysine methyltransferase regulates leukemia cell growth and regeneration after genotoxic stress.Oncotarget · 2017Article
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- SETDB1 mediated FosB expression increases the cell proliferation rate during anticancer drug therapy.BMB reports · 2016Article
- p73 promotes glioblastoma cell invasion by directly activating POSTN (periostin) expression.Oncotarget · 2016Article
- P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development.Cell death & disease · 2016Review
- PLK2 phosphorylates and inhibits enriched TAp73 in human osteosarcoma cells.Cancer medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enhanced resistance to chemotherapy has been correlated with high levels of Delta-Np73 (DNp73), an anti-apoptotic protein of the p53 tumor-suppressor family which inhibits the pro-apoptotic members such as p53 and TAp73. Although genotoxic drugs have been shown to induce DNp73 degradation, lack of mechanistic understanding of this process precludes strategies to enhance the targeting of DNp73 and improve treatment outcomes. Antizyme (Az) is a mediator of ubiquitin-independent protein degradation regulated by the polyamine biosynthesis pathway. We show here that acetylpolyamine oxidase (PAOX), a catabolic enzyme of this pathway, upregulates DNp73 levels by suppressing its degradation via the Az pathway. Conversely, downregulation of PAOX activity by siRNA-mediated knockdown or chemical inhibition leads to DNp73 degradation in an Az-dependent manner. PAOX expression is suppressed by several genotoxic drugs, via selected members of the activator protein-1 (AP-1) transcription factors, namely c-Jun, JunB and FosB, which are required for stress-mediated DNp73 degradation. Finally, chemical- and siRNA-mediated inhibition of PAOX significantly reversed the resistant phenotype of DNp73-overexpressing cancer cells to genotoxic drugs. Together, these data define a critical mechanism for the regulation of DNp73 abundance, and reveal that inhibition of PAOX could widen the therapeutic index of cytotoxic drugs and overcome DNp73-mediated chemoresistance in tumors.
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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.