ArticleScientific reports2016
Increased sensitivity of BRCA defective triple negative breast tumors to plumbagin through induction of DNA Double Strand Breaks (DSB).
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Integrated in silico and in vitro evaluation of Genistein and Apigenin as dual inhibitors of PARP1 and ESR1 in breast cancer.BMC pharmacology & toxicology · 2026Article
- Different Derivatives of Plumbagin Analogue: Bioavailability and Their Toxicity Studies.Food science & nutrition · 2025Review
- Association between single nucleotide polymorphisms of DNA repair genes (BRCA1, BRCA2, and PALB2) and breast cancer incidence in a subset of Iranian population.Hereditary cancer in clinical practice · 2025Article
- Perspectives on mechanistic implications of ROS inducers for targeting viral infections.European journal of pharmacology · 2021Article
- BRCA1 promoter hypermethylation in human placenta: a hidden link with β-hCG expression.Carcinogenesis · 2020Article
- Anticancer Effects and Mechanisms of Action of Plumbagin: Review of Research Advances.BioMed research international · 2020Review
- β-hCG-induced mutant BRCA1 ignites drug resistance in susceptible breast tissue.Carcinogenesis · 2019Article
- Plumbagin Ameliorates Collagen-Induced Arthritis by Regulating Treg/Th17 Cell Imbalances and Suppressing Osteoclastogenesis.Frontiers in immunology · 2018Article
- BRCA1 regulation on β-hCG: a mechanism for tumorigenicity in BRCA1 defective breast cancer.Oncogenesis · 2017Article
- Curcumin induces G2/M cell cycle arrest and apoptosis of head and neck squamous cell carcinomaOncotarget · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have earlier shown that Plumbagin (PB) can induce selective cytotoxicity to BRCA1 defective ovarian cancer cells; however, the effect of this molecule in BRCA1 mutated breast cancers has not been analyzed yet. Here, we report that reactive oxygen species (ROS) induced by PB resulted in DNA DSB and activates downstream signaling by ATR/ATM kinases and subsequent apoptosis. PB reduces DNA- dependent protein kinase (DNA-PK) expression and inhibits NHEJ (Non Homologous End Joining) activity in BRCA1 defective breast cancer cells. Also, PB induces apoptosis in two different BRCA1 conditional knock out murine models: MMTV-Cre; BRCA1(Co/Co) and WAP-Cre; BRCA1(Co/Co), at 2 mg/kg body weight, but 32 mg/kg of carboplatin (CN) was needed to induce apoptosis in them. This is the first study where two different tissue specific promoter driven transgenic mice models with BRCA1 exon 11 deletions are used for preclinical drug testing. The apoptosis induced by PB in HR (Homologous Recombination) defective triple negative BRCA1 mutant cell lines and in mouse models occur by inducing ROS mediated DNA DSB. The toxicity profile as compared with CN in transgenic mice provides evidence for PB's safer disposition as a therapeutic lead in breast cancer drug development.
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