ArticleCell cycle (Georgetown, Tex.)2014
BRCA1 as a nicotinamide adenine dinucleotide (NAD)-dependent metabolic switch in ovarian cancer.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Exploiting synthetic lethality in epithelial ovarian cancer: multi-dimensional approaches beyond DNA damage repair.Molecular cancer · 2026Review
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Relationship Between Thyroid Dysfunction and Ovarian Cancer.Biomolecules · 2025Review
- Biological Functions and Therapeutic Potential of NADCancers · 2024Review
- Supplementation with NAD+ and its precursors: A rescue of female reproductive diseases.Biochemistry and biophysics reports · 2024Review
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Article
- Review
- Prediction of Cervical Cancer Outcome by Identifying and Validating a NAD+ Metabolism-Derived Gene Signature.Journal of personalized medicine · 2022Article
- Plasma Metabolome Signature Indicative ofFrontiers in oncology · 2021Article
- Targeting MALAT1 induces DNA damage and sensitize non-small cell lung cancer cells to cisplatin by repressing BRCA1.Cancer chemotherapy and pharmacology · 2020Article
- Environmentally relevant exposure to dibutyl phthalate disrupts DNA damage repair gene expression in the mouse ovary†.Biology of reproduction · 2019Article
- Role of mitochondria in rescuing glycolytically inhibited subpopulation of triple negative but not hormone-responsive breast cancer cells.Scientific reports · 2019Article
- Circular RNA AKT3 upregulates PIK3R1 to enhance cisplatin resistance in gastric cancer via miR-198 suppression.Molecular cancer · 2019Article
- Beyond Energy Metabolism: Exploiting the Additional Roles of NAMPT for Cancer Therapy.Frontiers in oncology · 2019Review
- NAD Metabolism in Cancer Therapeutics.Frontiers in oncology · 2018Review
- On metabolic reprogramming and tumor biology: A comprehensive survey of metabolism in breast cancer.Oncotarget · 2016Review
- Effect of the BRCA1-SIRT1-EGFR axis on cisplatin sensitivity in ovarian cancer.American journal of translational research · 2016Article
- Linking BRCA1 to NAD World.Cell cycle (Georgetown, Tex.) · 2015Article
- Regulative Effect of Nampt on Tumor Progression and Cell Viability in Human Colorectal Cancer.Journal of Cancer · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both hereditary factors (e.g., BRCA1) and nicotinamide adenine dinucleotide (NAD)-dependent metabolic pathways are implicated in the initiation and progression of ovarian cancer. However, whether crosstalk exists between BRCA1 and NAD metabolism remains largely unknown. Here, we showed that: (i) BRCA1 inactivation events (mutation and promoter methylation) were accompanied by elevated levels of NAD; (ii) the knockdown or overexpression of BRCA1 was an effective way to induce an increase or decrease of nicotinamide phosphoribosyltransferase (Nampt)-related NAD synthesis, respectively; and (iii) BRCA1 expression patterns were inversely correlated with NAD levels in human ovarian cancer specimens. In addition, it is worth noting that: (i) NAD incubation induced increased levels of BRCA1 in a concentration-dependent manner; (ii) Nampt knockdown-mediated reduction in NAD levels was effective at inhibiting BRCA1 expression; and (iii) the overexpression of Nampt led to higher NAD levels and a subsequent increase in BRCA1 levels in primary ovarian cancer cells and A2780, HO-8910 and ES2 ovarian cancer cell lines. These results highlight a novel link between BRCA1 and NAD. Our findings imply that genetic (e.g., BRCA1 inactivation) and NAD-dependent metabolic pathways are jointly involved in the malignant progression of ovarian cancer.
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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.