ArticleCell cycle (Georgetown, Tex.)2014
A novel crosstalk between BRCA1 and poly (ADP-ribose) polymerase 1 in breast 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 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Characterization of Parthanatos in Breast Cancer: Implications for Prognosis and PARP Inhibitor Resistance.Bioengineering (Basel, Switzerland) · 2025Article
- Therapeutic Targeting of PARP Expression and Glycolysis Rate-Limiting Enzymes in Breast Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Article
- NetCellMatch: Multiscale Network-Based Matching of Cancer Cell Lines to Patients Using Graphical Wavelets.Chemistry & biodiversity · 2022Article
- Computational compensatory mutation discovery approach: Predicting a PARP1 variant rescue mutation.Biophysical journal · 2022Article
- Promoter Hypermethylation and Expression Changes of BRCA1 Gene in a Cohort of Sporadic Breast Cancer Cases among Pakistani Population.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Mitochondrial Deoxyguanosine Kinase Regulates NADFrontiers in oncology · 2020Article
- Mortaparib, a novel dual inhibitor of mortalin and PARP1, is a potential drug candidate for ovarian and cervical cancers.Journal of experimental & clinical cancer research : CR · 2019Article
- Expression of NAMPT is associated with breast invasive ductal carcinoma development and prognosis.Oncology letters · 2018Article
- A PET imaging agent for evaluating PARP-1 expression in ovarian cancer.The Journal of clinical investigation · 2018Article
- Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells.Cellular and molecular life sciences : CMLS · 2017Review
- 14-3-3σ Contributes to Radioresistance By Regulating DNA Repair and Cell Cycle via PARP1 and CHK2.Molecular cancer research : MCR · 2017Article
- FASN regulates cellular response to genotoxic treatments by increasing PARP-1 expression and DNA repair activity via NF-κB and SP1.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Nuclear PARP1 expression and its prognostic significance in breast cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Effect of the BRCA1-SIRT1-EGFR axis on cisplatin sensitivity in ovarian cancer.American journal of translational research · 2016Article
- Mutated Fanconi anemia pathway in non-Fanconi anemia cancers.Oncotarget · 2015Article
- Nicotinamide adenine dinucleotide (NAD) may affect DNA methyltransferase 1 through regulation of BRCA1 in ovarian cancer.American journal of cancer research · 2015Article
- Linking BRCA1 to NAD World.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA mutations are the main known hereditary factor for breast cancer. Notably, poly (ADP-ribose) polymerase 1 (PARP1) expression status plays a critical role in breast cancer progression and the clinical development of PARP1 inhibitors to treat BRCA-mutated breast cancer has advanced rapidly. However, dynamic crosstalk between BRCA1 and PARP1 remains largely unknown. Here, we showed that: (i) BRCA1 inactivation events (mutation, promoter methylation, or knockdown) were accompanied by increased PARP1 and nicotinamide adenine dinucleotide (NAD) levels, and a subsequent increase in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; (ii) the overexpression of BRCA1 resulted in decreased PARP1 and NAD levels, and a subsequent impairment in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; and (iii) intracellular NAD levels were largely responsible for regulating PARP1 activity in breast cancer cells, and NAD levels were positively correlated with PARP1 activity in human breast cancer specimens (R = 0.647, P < 0.001). Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion. These results highlight a novel interaction between BRCA1 and PARP1, which may be beneficial for the dynamic balance between BRCA1 and PARP1-related biologic processes, especially for maintaining stable DNA repair ability. All of this may improve our understanding of the basic molecular mechanism underlying BRCA1- and PARP1-related breast cancer progression.
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