ArticleBreast cancer research and treatment2016
Withaferin A inhibits in vivo growth of breast cancer cells accelerated by Notch2 knockdown.
Article in Breast cancer research and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Functional Gene Expression Differentiation of the Notch Signaling Pathway in Female Reproductive Tract Tissues-A Comprehensive Review With Analysis.Frontiers in cell and developmental biology · 2020Pooled it
- Notch receptors in breast cancer: context-dependent roles and therapeutic targeting.Cell communication and signaling : CCS · 2026Review
- Exploring the therapeutic potential of withaferin A by modulating key oncosignaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The role of Notch signalling and its crosstalk with oestrogen receptor signalling in breast cancer.Cancer metastasis reviews · 2026Review
- Mechanisms and potential therapeutic strategies of withaferin A in breast cancer.Pharmacological reports : PR · 2025Review
- Phytoconstituents as emerging therapeutics for breast cancer: Mechanistic insights and clinical implications.Cancer pathogenesis and therapy · 2025Review
- NOTCH1 combined with chemotherapy synergistically inhibits triple-negative breast cancer.World journal of clinical oncology · 2025Article
- Herbal Medicine in Breast Cancer Therapy: Mechanisms, Evidence, and Future Perspectives.Current issues in molecular biology · 2025Review
- Article
- Effects and mechanisms of exosomes in microenvironment angiogenesis in breast cancer: An updated review.Oncology research · 2025Review
- Review
- The Therapeutic Effects of Withaferin A against Cancer: Overview and Updates.Current molecular medicine · 2024Review
- Withaferin A: A Dietary Supplement with Promising Potential as an Anti-Tumor Therapeutic for Cancer Treatment - Pharmacology and Mechanisms.Drug design, development and therapy · 2023Review
- Tackling heterogeneity in treatment-resistant breast cancer using a broad-spectrum therapeutic approach.Cancer drug resistance (Alhambra, Calif.) · 2022Article
- Why is Mortalin a Potential Therapeutic Target for Cancer?Frontiers in cell and developmental biology · 2022Review
- Notch3 inhibits cell proliferation and tumorigenesis and predicts better prognosis in breast cancer through transactivating PTEN.Cell death & disease · 2021Article
- A Comprehensive Review and Perspective on Anticancer Mechanisms of Withaferin A in Breast Cancer.Cancer prevention research (Philadelphia, Pa.) · 2020Review
- Top Notch Targeting Strategies in Cancer: A Detailed Overview of Recent Insights and Current Perspectives.Cells · 2020Review
- Prenatal epigenetics diets play protective roles against environmental pollution.Clinical epigenetics · 2019Review
- Study of diffusion-weighted magnetic resonance imaging in the evaluation of the response to AAV2-VEGF-Trap neoadjuvant treatment in a triple-negative breast cancer animal model.Cancer medicine · 2019Article
Corrections and comments
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Authors and funding
12 authors.
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Abstract
The present study offers novel insights into the molecular circuitry of accelerated in vivo tumor growth by Notch2 knockdown in triple-negative breast cancer (TNBC) cells. Therapeutic vulnerability of Notch2-altered growth to a small molecule (withaferin A, WA) is also demonstrated. MDA-MB-231 and SUM159 cells were used for the xenograft studies. A variety of technologies were deployed to elucidate the mechanisms underlying tumor growth augmentation by Notch2 knockdown and its reversal by WA, including Fluorescence Molecular Tomography for measurement of tumor angiogenesis in live mice, Seahorse Flux analyzer for ex vivo measurement of tumor metabolism, proteomics, and Luminex-based cytokine profiling. Stable knockdown of Notch2 resulted in accelerated in vivo tumor growth in both cells reflected by tumor volume and/or latency. For example, the wet tumor weight from mice bearing Notch2 knockdown MDA-MB-231 cells was about 7.1-fold higher compared with control (P < 0.0001). Accelerated tumor growth by Notch2 knockdown was highly sensitive to inhibition by a promising steroidal lactone (WA) derived from a medicinal plant. Molecular underpinnings for tumor growth intensification by Notch2 knockdown included compensatory increase in Notch1 activation, increased cellular proliferation and/or angiogenesis, and increased plasma or tumor levels of growth stimulatory cytokines. WA administration reversed many of these effects providing explanation for its remarkable anti-cancer efficacy. Notch2 functions as a tumor growth suppressor in TNBC and WA offers a novel therapeutic strategy for restoring this function.
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