ArticleScientific reports2015
Copper depletion inhibits CoCl2-induced aggressive phenotype of MCF-7 cells via downregulation of HIF-1 and inhibition of Snail/Twist-mediated epithelial-mesenchymal transition.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 84 citations in OpenAlex.
- Unveiling the Impact of Copper Metabolism on Epithelial-Mesenchymal Transition of Triple-Negative Breast Cancer: Identification of Therapeutic Targets.Interdisciplinary sciences, computational life sciences · 2026Article
- Cuproptosis in prostate cancer: Molecular mechanisms, prognostic biomarkers and therapeutic frontiers of cuproptosis‑related genes (Review).International journal of oncology · 2025Review
- Integrating cuproptosis and immunosenescence: A novel therapeutic strategy in cancer treatment.Biochemistry and biophysics reports · 2025Review
- The molecular mechanism and therapeutic landscape of copper and cuproptosis in cancer.Signal transduction and targeted therapy · 2025Review
- Targeting cuproptosis for cancer therapy: Focus on the anti-tumor immune system.Cancer pathogenesis and therapy · 2025Review
- Cuproptosis-Related Gene FDX1 Suppresses the Growth and Progression of Colorectal Cancer by Retarding EMT Progress.Biochemical genetics · 2025Article
- Involvement of copper in cell death and cancer.Apoptosis : an international journal on programmed cell death · 2025Review
- Roles of Copper Transport Systems Members in Breast Cancer.Cancer medicine · 2024Review
- Detrimental interactions of hypoxia and complement MASP-1 in endothelial cells as a model for atherosclerosis-related diseases.Scientific reports · 2024Article
- Cuproptosis in lung cancer: mechanisms and therapeutic potential.Molecular and cellular biochemistry · 2024Review
- Intelligent gold nanocluster for effective treatment of malignant tumor via tumor-specific photothermal-chemodynamic therapy with AIE guidance.National science review · 2024Article
- Copper in Gynecological Diseases.International journal of molecular sciences · 2023Review
- Copper Exposure Induces Epithelial-Mesenchymal Transition-Related Fibrotic Change via Autophagy and Increase Risk of Lung Fibrosis in Human.Antioxidants (Basel, Switzerland) · 2023Article
- Investigations of cellular copper metabolism in ovarian cancer cells using a ratiometric fluorescent copper dye.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2023Article
- Copper homeostasis and cuproptosis in tumor pathogenesis and therapeutic strategies.Frontiers in pharmacology · 2023Review
- Copper in cancer: from limiting nutrient to therapeutic target.Frontiers in oncology · 2023Review
- Toxic metals in the regulation of epithelial-mesenchymal plasticity: demons or angels?Cancer cell international · 2022Review
- From Tissue Physoxia to Cancer Hypoxia, Cost-Effective Methods to Study Tissue-Specific OInternational journal of molecular sciences · 2022Article
- Reduced HIF-1α Stability Induced by 6-Gingerol Inhibits Lung Cancer Growth through the Induction of Cell Death.Molecules (Basel, Switzerland) · 2022Article
- Relationship between copper and immunity: The potential role of copper in tumor immunity.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper, a strictly regulated trace element, is essential for many physiological processes including angiogenesis. Dysregulated angiogenesis has been associated with increased copper in tumors, and thus copper chelators have been used to inhibit tumor angiogenesis. However, it remains unclear whether copper has any effect on epithelial-mesenchymal transition (EMT). Using CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhibited EMT-like cell morphology and cytoskeleton arrangement triggered by CoCl2; decreased the expression of vimentin and fibronectin, markers typical of EMT; inhibited HIF-1 activation and HIF1-α accumulation in nuclear; and down-regulated the expression of hypoxia-associated transcription factors, Snail and Twist1. Moreover, knockdown copper transport protein, Ctr1, also inhibited CoCl2-induced EMT and reversed the mesenchymal phenotype. In EMT6 xenograft mouse models, TEPA administration inhibited the tumor growth and increased mice survival. Immunohistochemical analysis of the xenograft further demonstrated that TEPA administration significantly inhibited tumor angiogenesis, down-regulated hypoxia-induced transcription factors, Snail and Twist1, leading to decreased transactivation of EMT-associated marker genes, vimentin and fibronectin. These results indicate that TEPA inhibits CoCl2-induced EMT most likely via HIF1-α-Snail/Twist signaling pathway, and copper depletion may be exploited as a therapeutic for breast cancer.
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