ArticleRedox biology2015
Redox-modulating agents target NOX2-dependent IKKε oncogenic kinase expression and proliferation in human breast cancer cell lines.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Transfer RNA-Derived Small RNA-5'tiRNAGln Drives HNRNPC Phase Separation to Promote Breast Cancer Bone Metastasis by Regulating IGF1R.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of Piezo1 increases the sensitivity of breast cancer to hyperthermia therapy.Open medicine (Warsaw, Poland) · 2024Article
- The Association between NADPH Oxidase 2 (NOX2) and Drug Resistance in Cancer.Current cancer drug targets · 2024Review
- Targeting M2 Macrophages with a Novel NADPH Oxidase Inhibitor.Antioxidants (Basel, Switzerland) · 2023Article
- ROS and miRNA Dysregulation in Ovarian Cancer Development, Angiogenesis and Therapeutic Resistance.International journal of molecular sciences · 2022Review
- Gentian violet induces apoptosis and ferroptosis via modulating p53 and MDM2 in hepatocellular carcinoma.American journal of cancer research · 2022Article
- 13Antioxidants (Basel, Switzerland) · 2021Article
- Mechanoactivation of NOX2-generated ROS elicits persistent TRPM8 CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Inhibiting the Activity of NADPH Oxidase in Cancer.Antioxidants & redox signaling · 2020Article
- Dual oxidase 1 and NADPH oxidase 2 exert favorable effects in cervical cancer patients by activating immune response.BMC cancer · 2019Article
- Dihydrotanshinone-Induced NOX5 Activation Inhibits Breast Cancer Stem Cell through the ROS/Stat3 Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- Analysis of the Effect of Gentian Violet on Apoptosis and Proliferation in Cutaneous T-Cell Lymphoma in an In Vitro Study.JAMA dermatology · 2018Article
- Paradoxical roles of dual oxidases in cancer biology.Free radical biology & medicine · 2017Review
- Detection of IKKε by immunohistochemistry in primary breast cancer: association with EGFR expression and absence of lymph node metastasis.BMC cancer · 2017Article
- Albendazole as a promising molecule for tumor control.Redox biology · 2016Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Oxidative stress is considered a causative factor in carcinogenesis, but also in the development of resistance to current chemotherapies. The appropriate usage of redox-modulating compounds is limited by the lack of knowledge of their impact on specific molecular pathways. Increased levels of the IKKε kinase, as a result of gene amplification or aberrant expression, are observed in a substantial number of breast carcinomas. IKKε not only plays a key role in cell transformation and invasiveness, but also in the development of resistance to tamoxifen. Here, we studied the effect of in vitro treatment with the redox-modulating triphenylmethane dyes, Gentian Violet and Brilliant Green, and nitroxide Tempol on IKKε expression and cell proliferation in the human breast cancer epithelial cell lines exhibiting amplification of IKKε, MCF-7 and ZR75.1. We show that Gentian Violet, Brilliant Green and Tempol significantly decrease intracellular superoxide anion levels and inhibit IKKε expression and cell viability. Treatment with Gentian Violet and Brilliant Green was associated with a reduced cyclin D1 expression and activation of caspase 3 and/or 7. Tempol decreased cyclin D1 expression in both cell lines, while activation of caspase 7 was only observed in MCF-7 cells. Silencing of the superoxide-generating NOX2 NADPH oxidase expressed in breast cancer cells resulted in the significant reduction of IKKε expression. Taken together, our results suggest that redox-modulating compounds targeting NOX2 could present a particular therapeutic interest in combination therapy against breast carcinomas exhibiting IKKε amplification.
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