ArticleOncogene2005
Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 346 citations in OpenAlex.
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- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- BRD4-mediated transcriptional activation of PDLIM4 enhances p21 stability and chemosensitivity in lung adenocarcinoma independent of p53.BMC biology · 2026Article
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- Luminescent Nanocucurbits Enable Spatiotemporal Co-Delivery of Hydrophilic and Hydrophobic Chemotherapeutic Agents.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of Lactate in Mitochondrial Metabolism of DOX-Induced Senescent AC16 Cells.Cell biochemistry and function · 2025Article
- Aurora Kinase A and B inhibition abrogates 'Neosis', a non-mitotic cell division of GBM residual cells and prevents GBM recurrence.Oncogene · 2025Article
- Substrate stiffness dictates unique doxorubicin-induced senescence-associated secretory phenotypes and transcriptomic signatures in human pulmonary fibroblasts.GeroScience · 2025Article
- Dual role of p21 in regulating apoptosis and mitotic integrity in response to doxorubicin in colon cancer cells.Cell death discovery · 2025Article
- VERU-111, an orally available tubulin inhibitor, suppresses ovarian tumor growth and metastasis.The Journal of pharmacology and experimental therapeutics · 2025Article
- Cancer therapy-related cardiovascular aging: mechanisms, monitoring, and intervention strategies.Frontiers in cardiovascular medicine · 2025Review
- N-Acetyl Cysteine as a promising therapeutic approach in ovarian cancer: potential and perspectives.Academia oncology · 2025Article
- HuR inhibition overcomes cFLIP-mediated doxorubicin resistance in triple-negative breast cancer.NPJ precision oncology · 2024Article
- Development and In-Vitro Evaluation of Doxorubicin-Loaded Methacrylate Gelatin (GelMa)-Acrylamide Hydrogels for the Treatment of Malignant Pleural Mesothelioma.Pharmaceutical research · 2024Article
- Substrate Stiffness Dictates Unique Doxorubicin-induced Senescence-associated Secretory Phenotypes and Transcriptomic Signatures in Human Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2024Article
- Photoactive metabolite mediated photodynamic therapy of Rhabdomyosarcoma cell lines using medicinal plants and Doxorubicin co-treatments.BMC complementary medicine and therapies · 2024Article
- Research progress on morphology and mechanism of programmed cell death.Cell death & disease · 2024Review
- Transformer-based spatial-temporal detection of apoptotic cell death in live-cell imaging.eLife · 2024Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic exposure of many human hepatoma cell lines to a low dose (LD) of doxorubicin induced a senescence-like phenotype (SLP) accompanied by enlargement of cells and increased senescence-associated beta-galactosidase activity. LD doxorubicin-induced SLP was preceded by multinucleation and downregulation of multiple proteins with mitotic checkpoint function, including CENP-A, Mad2, BubR1, and Chk1. LD doxorubicin-treated cells eventually underwent cell death through mitotic catastrophe. When we investigated whether LD doxorubicin-induced cell death shares biochemical characteristics with high dose (HD) doxorubicin-induced apoptosis in Huh-7 cells, we observed that externalization of phosphatidyl serine and release of mitochondrial cytochrome c into the cytosol was associated with both types of cell death. However, propidium iodide exclusion assays showed that membrane integrity was lost in the initial phase of LD doxorubicin-induced cell death through mitotic catastrophe, whereas it was lost during the late phase of HD doxorubicin-induced apoptosis. Furthermore, HD doxorubicin-induced apoptosis but not LD doxorubicin-induced mitotic catastrophe led to transient activation of NF-kappaB and strong, sustained activations of p38, c-Jun N-terminal kinase, and caspases. Collectively, these results indicate that different doses of doxorubicin activate different regulatory mechanisms to induce either apoptosis or cell death through mitotic catastrophe.
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