ArticleBioMed research international2015
Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
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- Yttrium oxide nanoparticles induce selective cytotoxicity, genomic instability and ROS mitochondrial P53 mediated apoptosis in human pancreatic cancer cells.Scientific reports · 2025Article
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- Synergistic Effect of Doxorubicin and Blue Light Irradiation on the Antitumor Treatment of HepG2 Cells in Liver Cancer.Molecules (Basel, Switzerland) · 2024Article
- NovelJournal of enzyme inhibition and medicinal chemistry · 2023Article
- Morin Sensitizes MDA-MB-231 Triple-Negative Breast Cancer Cells to Doxorubicin Cytotoxicity by Suppressing FOXM1 and Attenuating EGFR/STAT3 Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Targeted delivery of paclitaxel drug using polymer-coated magnetic nanoparticles for fibrosarcoma therapy: in vitro and in vivo studies.Scientific reports · 2023Article
- Anticancer Properties ofInternational journal of molecular sciences · 2022Article
- Anticancer Water-Soluble Organoruthenium Complexes: Synthesis and Preclinical Evaluation.Chembiochem : a European journal of chemical biology · 2022Article
- Synergistic effect of cold atmospheric pressure plasma and free or liposomal doxorubicin on melanoma cells.Scientific reports · 2021Article
- Relationship between Oxidative Stress and Imatinib Resistance in Model Chronic Myeloid Leukemia Cells.Biomolecules · 2021Article
- Nanoparticle delivery of a pH-sensitive prodrug of doxorubicin and a mitochondrial targeting VES-HScientific reports · 2020Article
- Developing Nanoceria-Based pH-Dependent Cancer-Directed Drug Delivery System for Retinoblastoma.Advanced functional materials · 2018Article
- MiR-122 Reverses the Doxorubicin-Resistance in Hepatocellular Carcinoma Cells through Regulating the Tumor Metabolism.PloS one · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Imatinib resistance is an emerging problem in the therapy of chronic myeloid leukemia (CML). Because imatinib induces apoptosis, which may be coupled with mitochondria and DNA damage is a prototype apoptosis-inducing factor, we hypothesized that imatinib-sensitive and -resistant CML cells might differentially express apoptosis-related mitochondrially encoded genes in response to genotoxic stress. We investigated the effect of doxorubicin (DOX), a DNA-damaging anticancer drug, on apoptosis and the expression of the mitochondrial NADH dehydrogenase 3 (MT-ND3) and cytochrome b (MT-CYB) in model CML cells showing imatinib resistance caused by Y253H mutation in the BCR-ABL1 gene (253) or culturing imatinib-sensitive (S) cells in increasing concentrations of imatinib (AR). The imatinib-resistant 253 cells displayed higher sensitivity to apoptosis induced by 1 μM DOX and this was confirmed by an increased activity of executioner caspases 3 and 7 in those cells. Native mitochondrial potential was lower in imatinib-resistant cells than in their sensitive counterparts and DOX lowered it. MT-CYB mRNA expression in 253 cells was lower than that in S cells and 0.1 μM DOX kept this relationship. In conclusion, imatinib resistance may be associated with altered mitochondrial response to genotoxic stress, which may be further exploited in CML therapy in patients with imatinib resistance.
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