ArticleJournal of cancer research and clinical oncology2013
Doxorubicin induces atypical NF-κB activation through c-Abl kinase activity in breast cancer cells.
Article in Journal of cancer research and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Synergistic Cytotoxicity of Cafestol and Kahweol With Doxorubicin in Breast Cancer Cells Involves TNF‑α Targeting and NF‑κB Downregulation.Archiv der Pharmazie · 2026Article
- Emerging Targets and Treatments for Doxorubicin-Induced Cardiac Inflammation.Journal of inflammation research · 2026Review
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- Chemotherapy-initiated cysteine-rich protein 61 decreases acute B-lymphoblastic leukemia chemosensitivity.Journal of cancer research and clinical oncology · 2024Article
- Triple Reporter Assay: A Non-Overlapping Luciferase Assay for the Measurement of Complex Macromolecular Regulation in Cancer Cells Using a New Mushroom Luciferase-Luciferin Pair.Sensors (Basel, Switzerland) · 2023Article
- Curcumin as an Enhancer of Therapeutic Efficiency of Chemotherapy Drugs in Breast Cancer.International journal of molecular sciences · 2022Review
- IL-17A Increases Doxorubicin Efficacy in Triple Negative Breast Cancer.Frontiers in oncology · 2022Article
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- Antimicrobial Peptide againstPharmaceutics · 2020Article
- Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer.Frontiers in oncology · 2020Review
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- Metformin reverses mesenchymal phenotype of primary breast cancer cells through STAT3/NF-κB pathways.BMC cancer · 2019Article
- Insights into the transcriptional regulation of the anthracycline reductase AKR7A2 in human cardiomyocytes.Toxicology letters · 2019Article
- Activation of NF-κB in B cell receptor signaling through Bruton's tyrosine kinase-dependent phosphorylation of IκB-α.Journal of molecular medicine (Berlin, Germany) · 2019Article
- A Practical Review of Proteasome Pharmacology.Pharmacological reviews · 2019Review
- Ginger extract adjuvant to doxorubicin in mammary carcinoma: study of some molecular mechanisms.European journal of nutrition · 2018Article
- Cellular stress response mechanisms of Rhizoma coptidis: a systematic review.Chinese medicine · 2018Review
- Next-generation proteasome inhibitor oprozomib enhances sensitivity to doxorubicin in triple-negative breast cancer cells.International journal of clinical and experimental pathology · 2018Article
- Involvement of c-Abl Kinase in Microglial Activation of NLRP3 Inflammasome and Impairment in Autolysosomal System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- Global Regulation of Differential Gene Expression by c-Abl/Arg Oncogenic Kinases.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeNF-κB transcription factor has been associated with cancer development and chemoresistance. We studied the signaling pathway activated by doxorubicin (DOX) leading to NF-κB activation in breast cancer cells.
methodsNF-κB activity was evaluated by electrophoretic mobility shift in T47D, ZR75.30 and primary culture (MBCDF) from a ductal infiltrating carcinoma. Cell viability was measured by crystal violet. Western blotting was performed to check the expression and phosphorylation of IκBα Ser-32/36. c-Abl was inhibited with Imatinib or by overexpressing a dominant negative form of c-Abl (K290R).
resultsWe found a correlation between sensitivity to DOX and amplitude of NF-κB activation. In cells least sensitive to DOX, NF-κB remained activated for longer time (T47D and MBCDF). The opposite effect was observed in cells sensitive to DOX (ZR75.30). DOX did not induce IκBα degradation or Ser-32/36 phosphorylation. Instead, there were modifications in the levels of IκBα tyrosine phosphorylation, suggesting an atypical NF-κB activation. In DOX-resistant cells, Imatinib treatment reduced IκBα tyrosine phosphorylation and NF-κB activity. The Imatinib-DOX combination significantly enhanced cell death of T47D and MBCDF breast cancer cells. Overexpression of c-Abl K290R in T47D and MBCDF cells reduced basal and DOX-induced NF-κB activation as well as IκBα tyrosine phosphorylation. In c-Abl K290R cells, DOX treatment did not mimic the combination Imatinib-DOX-induced cell death.
conclusionsInhibition of c-Abl inactivated IκBα/NF-κB pathway is associated with IκBα tyrosine phosphorylation in breast cancer cells. These results also raise the potential use of a combined therapy with Imatinib and DOX for breast cancer patients.
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