ArticleOncotarget2014
The DNA2 nuclease/helicase is an estrogen-dependent gene mutated in breast and ovarian cancers.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Multi-omics analysis positions DNA2 at the interface of genome integrity programs and tumor behavior in pan-cancer.Functional & integrative genomics · 2026Article
- Article
- Estrogen upregulates DNA2 expression through the PI3K-AKT pathway in endometrial carcinoma.Journal of Zhejiang University. Science. B · 2023Article
- Review
- TheGenes · 2022Article
- Up-regulation of DNA2 results in cell proliferation and migration in endometriosis.Journal of molecular histology · 2021Article
- Review
- Genome-Wide Analysis Unveils DNA Helicase RECQ1 as a Regulator of Estrogen Response Pathway in Breast Cancer Cells.Molecular and cellular biology · 2021Article
- Decoding Cancer Variants of Unknown Significance for Helicase-Nuclease-RPA Complexes Orchestrating DNA Repair During Transcription and Replication.Frontiers in molecular biosciences · 2021Article
- Increased Expression of DNA2 Was Linked to Poor Prognosis in Breast Cancer.Disease markers · 2021Article
- Limiting homologous recombination at stalled replication forks is essential for cell viability: DNA2 to the rescue.Current genetics · 2020Review
- Disease-associated DNA2 nuclease-helicase protects cells from lethal chromosome under-replication.Nucleic acids research · 2020Article
- Multiple roles of DNA2 nuclease/helicase in DNA metabolism, genome stability and human diseases.Nucleic acids research · 2020Review
- Article
- Review
- A Critical Role for Dna2 at Unwound Telomeres.Genetics · 2018Article
- DNA2-An Important Player in DNA Damage Response or Just Another DNA Maintenance Protein?International journal of molecular sciences · 2017Review
- Article
- Inhibition of DNA2 nuclease as a therapeutic strategy targeting replication stress in cancer cells.Oncogenesis · 2017Article
- Replication intermediates that escape Dna2 activity are processed by Holliday junction resolvase Yen1.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic instability, a hallmark of cancer, is commonly caused by failures in the DNA damage response. Here we conducted a bioinformatical screen to reveal DNA damage response genes that are upregulated by estrogen and highly mutated in breast and ovarian cancers. This screen identified 53 estrogen-dependent cancer genes, some of which are novel. Notably, the screen retrieved 9 DNA helicases as well as 5 nucleases. DNA2, which functions as both a helicase and a nuclease and plays a role in DNA repair and replication, was retrieved in the screen. Mutations in DNA2, found in estrogen-dependent cancers, are clustered in the helicase and nuclease domains, suggesting activity impairment. Indeed, we show that mutations found in ovarian cancers impair DNA2 activity. Depletion of DNA2 in cells reduces their tumorogenicity in mice. In human, high expression of DNA2 correlates with poor survival of estrogen receptor-positive patients but not of estrogen receptor-negative patients. We also demonstrate that depletion of DNA2 in cells reduces proliferation, while addition of estrogen restores proliferation. These findings suggest that cells responding to estrogen will proliferate despite impaired in DNA2 activity, potentially promoting genomic instability and triggering cancer development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.