ArticleCell death & disease2017
Withaferin-A kills cancer cells with and without telomerase: chemical, computational and experimental evidences.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- Prokaryotic Molecular Defense Mechanisms and Their Potential Applications in Cancer Biology: A Special Consideration for Cyanobacterial Systems.Current issues in molecular biology · 2026Review
- Current mechanistic insights into Withaferin A: a promising potential adjuvant anticancer agent from Withania somnifera.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Molecular Characterization of Cancer Preventive and Therapeutic Potential of Three Antistress Compounds, Triethylene Glycol, Withanone, and Withaferin A.International journal of molecular sciences · 2025Article
- Molecular Insights into the Anticancer Activity of Withaferin-A: The Inhibition of Survivin Signaling.Cancers · 2024Article
- Telomerase Inhibition in the Treatment of Leukemia: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of Withaferin-A, Withanone, and Caffeic Acid Phenethyl Ester on DNA Methyltransferases: Potential in Epigenetic Cancer Therapy.Current topics in medicinal chemistry · 2024Article
- Anti-COVID-19 Potential of Withaferin-A and Caffeic Acid Phenethyl Ester.Current topics in medicinal chemistry · 2024Article
- Targeting Telomere Dynamics as an Effective Approach for the Development of Cancer Therapeutics.International journal of nanomedicine · 2024Review
- Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal PlantPharmaceuticals (Basel, Switzerland) · 2023Review
- Bioactivity-guided fractionation ofFrontiers in cell and developmental biology · 2023Article
- Review
- Computational Identification of BCR-ABL Oncogenic Signaling as a Candidate Target of Withaferin A and Withanone.Biomolecules · 2022Article
- Article
- Preparation, Characterization, and Pharmacological Investigation of Withaferin-A Loaded Nanosponges for Cancer Therapy; In Vitro, In Vivo and Molecular Docking Studies.Molecules (Basel, Switzerland) · 2021Article
- Effect of Ashwagandha Withanolides on Muscle Cell Differentiation.Biomolecules · 2021Article
- Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells.Scientific reports · 2021Article
- Computational Insights into the Potential of Withaferin-A, Withanone and Caffeic Acid Phenethyl Ester for Treatment of Aberrant-EGFR Driven Lung Cancers.Biomolecules · 2021Article
- Potential of Withaferin-A, Withanone and Caffeic Acid Phenethyl ester as ATP-competitive inhibitors of BRAF: A bioinformatics study.Current research in structural biology · 2021Article
- Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its Derivatives.Biomedicines · 2020Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance of telomere length is the most consistent attribute of cancer cells. Tightly connected to their capacity to overcome replicative mortality, it is achieved either by activation of telomerase or an Alternative mechanism of Lengthening of Telomeres (ALT). Disruption of either of these mechanisms has been shown to induce DNA damage signalling leading to senescence or apoptosis. Telomerase inhibitors are considered as potential anticancer drugs but are ineffective for ALT cancers (~15% of all cancers). Withaferin-A (Wi-A), a major constituent of the medicinal plant, Withania somnifera (Ashwagandha), has been shown to exert anti-tumour activity. However, its effect on either telomerase or ALT mechanisms has not been investigated. Here, by using isogenic cancer cells with/without telomerase, we found that Wi-A caused stronger cytotoxicity to ALT cells. It was associated with inhibition of ALT-associated promyelocytic leukemia nuclear bodies, an established marker of ALT. Comparative analyses of telomerase positive and ALT cells revealed that Wi-A caused stronger telomere dysfunction and upregulation of DNA damage response in ALT cells. Molecular computational and experimental analyses revealed that Wi-A led to Myc-Mad mediated transcriptional suppression of NBS-1, an MRN complex protein that is an essential component of the ALT mechanism. The results suggest that Wi-A could be a new candidate drug for ALT cancers.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.