ArticleBreast cancer research : BCR2005
Differential responses to doxorubicin-induced phosphorylation and activation of Akt in human breast cancer cells.
Article in Breast cancer research : BCR, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 100 citations in OpenAlex.
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- Dox-HCl and miR-145 co-delivery through CD44-targeted PEGylated liposomes inhibit Breast CancerNanomedicine (London, England) · 2025Article
- Spheroid Model of Mammary Tumor Cells: Epithelial-Mesenchymal Transition and Doxorubicin Response.Biology · 2024Article
- Effect of quercetin on doxorubicin cytotoxicity in sensitive and resistant human MCF7 breast cancer cell lines.Biomedical reports · 2024Article
- Doxorubicin and folic acid-loaded zinc oxide nanoparticles-based combined anti-tumor and anti-inflammatory approach for enhanced anti-cancer therapy.BMC cancer · 2024Article
- Thymoquinone Nanoparticle Induces Apoptosis and Cell Migration Retardation through Modulating of SUMOylation Process Genes in Breast Cancer Cell Line.Iranian journal of biotechnology · 2024Article
- Single-Cell Proliferation Microfluidic Device for High Throughput Investigation of Replicative Potential and Drug Resistance of Cancer Cells.Cellular and molecular bioengineering · 2023Article
- Protease-activated receptor 2 attenuates doxorubicin-induced apoptosis in colon cancer cells.Journal of cell communication and signaling · 2023Article
- The Essential Oil fromPharmaceuticals (Basel, Switzerland) · 2023Article
- LncRNA CASC2 Inhibits Progression of Glioblastoma by Regulating the Expression of AKT in T98G Cell Line, Treated by TMZ and Thiosemicarbazone Complex.Asian Pacific journal of cancer prevention : APJCP · 2023Article
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- CXCR2 Small-Molecule Antagonist Combats Chemoresistance and Enhances Immunotherapy in Triple-Negative Breast Cancer.Frontiers in pharmacology · 2022Article
- Pharmacologic inhibition of Akt in combination with chemotherapeutic agents effectively induces apoptosis in ovarian and endometrial cancer cell lines.Molecular oncology · 2021Article
- Targeted inhibition of cooperative mutation- and therapy-induced AKT activation in AML effectively enhances response to chemotherapy.Leukemia · 2021Article
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- Total saponins of Bolbostemma paniculatum (maxim.) Franquet exert antitumor activity against MDA-MB-231 human breast cancer cells via inhibiting PI3K/Akt/mTOR pathway.BMC complementary and alternative medicine · 2019Article
- Article
- Mechanisms of doxorubicin-induced drug resistance and drug resistant tumour growth in a murine breast tumour model.BMC cancer · 2019Article
- Insights into the transcriptional regulation of the anthracycline reductase AKR7A2 in human cardiomyocytes.Toxicology letters · 2019Article
- Inhibition of SHP2 by new compounds induces differential effects on RAS/RAF/ERK and PI3K/AKT pathways in different cancer cell types.Investigational new drugs · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionWe have shown previously that overexpression of constitutively active Akt or activation of Akt caused by constitutively active Ras or human epidermal growth factor receptor-2 (HER2) confers on breast cancer cells resistance to chemotherapy or radiotherapy. As an expanded study we here report differential responses in terms of phosphorylation and activation of Akt as a result of treatment with doxorubicin in a panel of breast cancer cell lines.
methodsThe levels of Akt phosphorylation and activity were measured by Western blot analysis with an anti-Ser473-phosphorylated Akt antibody and by in vitro Akt kinase assay using glycogen synthase kinase-3 as a substrate.
resultsWithin 24 hours after exposure to doxorubicin, MCF7, MDA468 and T47D cells showed a drug-dose-dependent increase in the levels of phosphorylated Akt; in contrast, SKBR3 and MDA231 cells showed a decrease in the levels of phosphorylated Akt, and minimal or no changes were detected in MDA361, MDA157 and BT474 cells. The doxorubicin-induced Akt phosphorylation was correlated with increased kinase activity and was dependent on phosphoinositide 3-kinase (PI3-K). An increased baseline level of Akt was also found in MCF7 cells treated with ionizing radiation. The cellular responses to doxorubicin-induced Akt phosphorylation were potentiated after the expression of Akt upstream activators including HER2, HER3 and focal adhesion kinase.
conclusionTaken together with our recent published results showing that constitutive Akt mediates resistance to chemotherapy or radiotherapy, our present data suggest that the doxorubicin-induced phosphorylation and activation of Akt might reflect a cellular defensive mechanism of cancer cells to overcome doxorubicin-induced cytotoxic effects, which further supports the current efforts of targeting PI3-K/Akt for enhancing the therapeutic responses of breast cancer cells to chemotherapy and radiotherapy.
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