ArticleBreast cancer research and treatment2012
ErbB1/2 tyrosine kinase inhibitor mediates oxidative stress-induced apoptosis in inflammatory breast cancer cells.
Article in Breast cancer research and treatment, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Altered ribosomal profile in acquired resistance and reversal associates with pathological response to chemotherapy in inflammatory breast cancer.NPJ breast cancer · 2024Article
- Identification and validation of a novel prognostic signature based on mitochondria and oxidative stress related genes for glioblastoma.Journal of translational medicine · 2023Article
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- Adaptive stress response genes associated with breast cancer subtypes and survival outcomes reveal race-related differences.NPJ breast cancer · 2022Article
- High dimensionality reduction by matrix factorization for systems pharmacology.Briefings in bioinformatics · 2022Article
- Tweaking EMT and MDR dynamics to constrain triple-negative breast cancer invasiveness by EGFR and Wnt/β-catenin signaling regulation.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- A polycyclic aromatic hydrocarbon-enriched environmental chemical mixture enhances AhR, antiapoptotic signaling and a proliferative phenotype in breast cancer cells.Carcinogenesis · 2020Article
- The Double-Faced Role of Nitric Oxide and Reactive Oxygen Species in Solid Tumors.Antioxidants (Basel, Switzerland) · 2020Review
- Neuroprotective Effects of the Anti-cancer Drug Lapatinib Against Epileptic Seizures via Suppressing Glutathione Peroxidase 4-Dependent Ferroptosis.Frontiers in pharmacology · 2020Article
- Development and implementation of the SUM breast cancer cell line functional genomics knowledge base.NPJ breast cancer · 2020Article
- Teaching the basics of reactive oxygen species and their relevance to cancer biology: Mitochondrial reactive oxygen species detection, redox signaling, and targeted therapies.Redox biology · 2018Review
- XIAP Regulation by MNK Links MAPK and NFκB Signaling to Determine an Aggressive Breast Cancer Phenotype.Cancer research · 2018Article
- The Influence of Metabolism on Drug Response in Cancer.Frontiers in oncology · 2018Review
- Pharmacological targeting of GLI1 inhibits proliferation, tumor emboli formation and in vivo tumor growth of inflammatory breast cancer cells.Cancer letters · 2017Article
- A c-Jun N-terminal kinase inhibitor, JNK-IN-8, sensitizes triple negative breast cancer cells to lapatinib.Oncotarget · 2017Article
- Potential for a novel manganese porphyrin compound as adjuvant canine lymphoma therapy.Cancer chemotherapy and pharmacology · 2017Article
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- Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy.Oxidative medicine and cellular longevity · 2017Review
- Lapatinib resistance in HER2+ cancers: latest findings and new concepts on molecular mechanisms.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Overexpression of epidermal growth factor receptors (ErbB) is frequently seen in inflammatory breast cancer (IBC). Treatment with ErbB1/2-targeting agents (lapatinib) mediates tumor apoptosis by downregulating ErbB1/2 phosphorylation and downstream survival signaling. In this study, using carboxy-H(2)DCFDA, DHE, and MitoSOX Red to examine changes in hydrogen peroxide radicals, cytoplasmic and mitochondrial superoxide, respectively, we observed that GW583340 (a lapatinib-analog) increases reactive oxygen species (ROS) in two models of IBC (SUM149, SUM190) that are sensitive to ErbB1/2 blockade. This significant increase in ROS levels was similar to those generated by classical oxidative agents H(2)O(2) and paraquat. In contrast, minimal to basal levels of ROS were measured in a clonal population of GW583340-resistant IBC cells (rSUM149 and rSUM190). The GW583340-resistant IBC cells displayed increased SOD1, SOD2, and glutathione expression, which correlated with decreased sensitivity to the apoptotic-inducing effects of GW583340, H(2)O(2), and paraquat. The ROS increase and cell death in the GW583340-sensitive cells was reversed by simultaneous treatment with a superoxide dismutase (SOD) mimic. Additionally, overcoming the high levels of antioxidants using redox modulators induced apoptosis in the GW583340-resistant cells. Taken together, these data demonstrate a novel mechanism of lapatinib-analog-induced apoptosis and indicate that resistant cells have increased antioxidant potential, which can be overcome by treatment with SOD modulators.
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Registered trials
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