ArticleLeukemia2009
Activation of p53 by Nutlin-3a, an antagonist of MDM2, induces apoptosis and cellular senescence in adult T-cell leukemia cells.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 71 citations in OpenAlex.
- FDXR upregulation by p63/p73 is a prognostic and therapeutic marker of adult T-cell leukemia/lymphoma.EMBO molecular medicine · 2026Article
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- TIGAR coordinates senescence-associated secretory phenotype via lysosome repositioning and α-tubulin deacetylation.Experimental & molecular medicine · 2024Article
- Nanoencapsulation of MDM2 Inhibitor RG7388 and Class-I HDAC Inhibitor Entinostat Enhances their Therapeutic Potential Through Synergistic Antitumor Effects and Reduction of Systemic Toxicity.Molecular pharmaceutics · 2024Article
- The potential for senotherapy as a novel approach to extend life quality in veterinary medicine.Frontiers in veterinary science · 2024Review
- 7-Geranyloxcycoumarin enhances radio sensitivity in human prostate cancer cells.Molecular biology reports · 2023Article
- The X-linked epigenetic regulator UTX controls NK cell-intrinsic sex differences.Nature immunology · 2023Article
- Alvocidib inhibits IRF4 expression via super-enhancer suppression and adult T-cell leukemia/lymphoma cell growth.Cancer science · 2022Article
- Do Bacteria Provide an Alternative to Cancer Treatment and What Role Does Lactic Acid Bacteria Play?Microorganisms · 2022Review
- Resistance mechanisms to inhibitors of p53-MDM2 interactions in cancer therapy: can we overcome them?Cellular & molecular biology letters · 2021Review
- TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Is Upregulated in Lymphocytes Stimulated with Concanavalin A.International journal of molecular sciences · 2021Article
- Cellular senescence and cancer: Focusing on traditional Chinese medicine and natural products.Cell proliferation · 2020Review
- Prognosis, Biology, and Targeting ofCells · 2020Review
- The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML Cells.Cancer discovery · 2019Article
- Essential genes shape cancer genomes through linear limitation of homozygous deletions.Communications biology · 2019Article
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Fructose 2,6-Bisphosphate in Cancer Cell Metabolism.Frontiers in oncology · 2018Review
- Caffeine Sensitizes U87-MG Human Glioblastoma Cells to Temozolomide through Mitotic Catastrophe by Impeding G2 Arrest.BioMed research international · 2018Article
- Expression of miR-34a in T-Cells Infected by Human T-Lymphotropic Virus 1.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that the induction of cellular senescence through p53 activation is an effective strategy in tumor regression. Unfortunately, however, tumors including adult T-cell leukemia/lymphoma (ATL) have disadvantages such as p53 mutations and a lack of p16(INK4a) and/or p14(ARF). In this study we characterized Nutlin-3a-induced cell death in 16 leukemia/lymphoma cell lines. Eight cell lines, including six ATL-related cell lines, had wild-type p53 and Nutlin-3a-activated p53, and the cell lines underwent apoptosis or cell-cycle arrest, whereas eight cell lines with mutated p53 were resistant. Interestingly, senescence-associated-beta-galactosidase (SA-beta-gal) staining revealed that only ATL-related cell lines with wild-type p53 showed cellular senescence, although they lack both p16(INK4a) and p14(ARF). These results indicate that cellular senescence is an important event in p53-dependent cell death in ATL cells and is inducible without p16(INK4a) and p14(ARF). Furthermore, knockdown of Tp53-induced glycolysis and apoptosis regulator (TIGAR), a novel target gene of p53, by small interfering RNA(siRNA) indicated its important role in the induction of cellular senescence. As many patients with ATL carry wild-type p53, our study suggests that p53 activation by Nutlin-3a is a promising strategy in ATL. We also found synergism with a combination of Nutlin-3a and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), suggesting the application of Nutlin-3a-based therapy to be broader than expected.
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Registered trials
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