ArticleOncotarget2015
Molecular mechanisms of cisplatin cytotoxicity in acute promyelocytic leukemia cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- The Chemoprotective Potentials of Alpha-lipoic Acid against Cisplatin-induced Ototoxicity: A Systematic Review.Current medicinal chemistry · 2024Pooled it
- Chemotherapy-Mediated Purging Before Testicular Organoid Generation Significantly Reduces Cancer Cells While Not Significantly Reducing Germ Cells.International journal of molecular sciences · 2026Article
- Mechanistic Insights intoInternational journal of molecular sciences · 2026Article
- Anticancer Effects of Fluphenazine Alone and in Combination with Cisplatin in Gastric Cancer Cells and a Mouse Xenograft Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Plumbagin sensitizes leukemia cells to cisplatin by promoting oxidative stress, apoptosis, and DNA damage.International journal of medical sciences · 2026Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Exosomes derived from bone marrow mesenchymal stem cells ameliorate chemotherapeutically induced damage in rats' parotid salivary gland.Oral and maxillofacial surgery · 2025Article
- Apoptotic cell death of stomach cancer lines (AGS) induced by Co-NTB complex through cellular organelles and DNA damage.RSC advances · 2025Article
- Collaboration ofFuture science OA · 2024Article
- Polysaccharides fromMolecular medicine reports · 2023Article
- Article
- Cisplatin Induces Apoptosis in Mouse Neonatal Testes Organ Culture.International journal of molecular sciences · 2022Article
- COPS5 Conferred the Platinum Resistance in Epithelial Ovarian Cancer.Current issues in molecular biology · 2022Article
- p53 as a unique target of action of cisplatin in acute leukaemia cells.Journal of cellular and molecular medicine · 2022Article
- Safety and efficacy of Compound Huangdai Tablets combined with all-trans retinoic acid for treatment of acute promyelocytic leukemia: Clinical evidence and potential mechanisms.Chinese herbal medicines · 2022Article
- Advances in Our Understanding of the Molecular Mechanisms of Action of Cisplatin in Cancer Therapy.Journal of experimental pharmacology · 2021Review
- Protein Carbonylation and Lipid Peroxidation in Hematological Malignancies.Antioxidants (Basel, Switzerland) · 2020Review
- Single-cell analysis of AIMP2 splice variants informs on drug sensitivity and prognosis in hematologic cancer.Communications biology · 2020Article
- Article
- Trisenox Disrupts MDM2-DAXX-HAUSP Complex and Induces Apoptosis in a Mouse Model of Acute Leukemia.Journal of Cancer · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cis-diamminedichloroplatinum (II) (cisplatin) is a widely used anti-tumor drug for the treatment of a broad range of human malignancies with successful therapeutic outcomes for head and neck, ovarian, and testicular cancers. It has been found to inhibit cell cycle progression and to induce oxidative stress and apoptosis in acute promyelocytic leukemia (APL) cells. However, its molecular mechanisms of cytotoxic action are poorly understood. We hypothesized that cisplatin induces cytotoxicity through DNA adduct formation, oxidative stress, transcriptional factors (p53 and AP-1), cell cycle regulation, stress signaling and apoptosis in APL cells. We used the APL cell line as a model, and applied a variety of molecular tools to elucidate the cytotoxic mode of action of cisplatin. We found that cisplatin inhibited cell proliferation by a cytotoxicity, characterized by DNA damage and modulation of oxidative stress. Cisplatin also activated p53 and phosphorylated activator protein (AP-1) component, c-Jun at serine (63, 73) residue simultaneously leading to cell cycle arrest through stimulation of p21 and down regulation of cyclins and cyclin dependent kinases in APL cell lines. It strongly activated the intrinsic pathway of apoptosis through alteration of the mitochondrial membrane potential, release of cytochrome C, and up-regulation of caspase 3 activity. It also down regulated the p38MAPK pathway. Overall, this study highlights the molecular mechanisms that underline cisplatin toxicity to APL cells, and provides insights into selection of novel targets and/or design of therapeutic agents to treat APL.
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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.