ArticleThe Journal of pathology2014
Up-regulation of the interferon-related genes in BRCA2 knockout epithelial cells.
Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting PARP-1 and DNA Damage Response Defects in Colorectal Cancer Chemotherapy with Established and Novel PARP Inhibitors.Cancers · 2024Article
- A transcriptional response to replication stress selectively expands a subset of Brca2-mutant mammary epithelial cells.Nature communications · 2023Article
- DNA-PK inhibition extends the therapeutic effects of Top2 poisoning to non-proliferating cells, increasing activity at a cost.Scientific reports · 2023Article
- Exploiting RIG-I-like receptor pathway for cancer immunotherapy.Journal of hematology & oncology · 2023Review
- Anti-tumoural activity of the G-quadruplex ligand pyridostatin against BRCA1/2-deficient tumours.EMBO molecular medicine · 2022Article
- Identifying Biomarkers of Alzheimer's Disease via a Novel Structured Sparse Canonical Correlation Analysis Approach.Journal of molecular neuroscience : MN · 2022Article
- An In-Depth Review of Niraparib in Ovarian Cancer: Mechanism of Action, Clinical Efficacy and Future Directions.Oncology and therapy · 2021Review
- Patients with BRCA mutated ovarian cancer may have fewer circulating MDSC and more peripheral CD8Oncology letters · 2019Article
- BRCA2 abrogation triggers innate immune responses potentiated by treatment with PARP inhibitors.Nature communications · 2019Article
- Chlorambucil targets BRCA1/2-deficient tumours and counteracts PARP inhibitor resistance.EMBO molecular medicine · 2019Article
- DNA Repair Deficiency in Breast Cancer: Opportunities for Immunotherapy.Journal of oncology · 2019Review
- The synthetic histone-binding regulator protein PcTF activates interferon genes in breast cancer cells.BMC systems biology · 2018Article
- BRCA1 Mutation Status and Follicular Fluid Exposure Alters NFκB Signaling and ISGylation in Human Fallopian Tube Epithelial Cells.Neoplasia (New York, N.Y.) · 2018Article
- Article
- CX-5461 is a DNA G-quadruplex stabilizer with selective lethality in BRCA1/2 deficient tumours.Nature communications · 2017Article
- Activation of IFN/STAT1 signalling predicts response to chemotherapy in oestrogen receptor-negative breast cancer.British journal of cancer · 2016Article
- G-quadruplex DNA as a molecular target for induced synthetic lethality in cancer cells.Journal of the American Chemical Society · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
BRCA2 mutations are significantly associated with early-onset breast cancer, and the tumour-suppressing function of BRCA2 has been attributed to its involvement in homologous recombination (HR)-mediated DNA repair. In order to identify additional functions of BRCA2, we generated BRCA2-knockout HCT116 human colorectal carcinoma cells. Using genome-wide microarray analyses, we have discovered a link between the loss of BRCA2 and the up-regulation of a subset of interferon (IFN)-related genes, including APOBEC3F and APOBEC3G. The over-expression of IFN-related genes was confirmed in different human BRCA2(-/-) and mouse Brca2(-/-) tumour cell lines, and was independent of senescence and apoptosis. In isogenic wild-type BRCA2 cells, we observed over-expression of IFN-related genes after treatment with DNA-damaging agents, and following ionizing radiation. Cells with endogenous DNA damage because of defective BRCA1 or RAD51 also exhibited over-expression of IFN-related genes. Transcriptional activity of the IFN-stimulated response element (ISRE) was increased in BRCA2 knockout cells, and the expression of BRCA2 greatly decreased IFNα-stimulated ISRE reporter activity, suggesting that BRCA2 directly represses the expression of IFN-related genes through the ISRE. Finally, the colony-forming capacity of BRCA2 knockout cells was significantly reduced in the presence of either IFNβ or IFNγ, suggesting that IFNs may have potential as therapeutic agents in cancer cells with BRCA2 mutations. The GEO Accession No. for microarray analysis is GSE54830.
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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.