ArticleOncogene2003
Overexpression of a protein fragment of RNA helicase A causes inhibition of endogenous BRCA1 function and defects in ploidy and cytokinesis in mammary epithelial cells.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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Who cites it
54 citing papers in PubMed, 101 citations in OpenAlex.
- Functional Disruption of IQGAP1 by Truncated PALB2 in Two Cases of Breast Cancer: Implications for Proliferation and Invasion.Biomedicines · 2025Article
- Established and Emerging Roles of DEAD/H-Box Helicases in Regulating Infection and Immunity.Immunological reviews · 2025Review
- The Impact of Centrosome Pathologies on Ovarian Cancer Development and Progression with a Focus on Centrosomes as Therapeutic Target.Advances in experimental medicine and biology · 2024Review
- Blocking tri-methylguanosine synthase 1 (TGS1) stops anchorage-independent growth of canine sarcomas.Cancer gene therapy · 2023Article
- Multiplexed assay of variant effect reveals residues of functional importance in the BRCA1 coiled-coil and serine cluster domains.PloS one · 2023Article
- A pan-cancer analysis of the expression and molecular mechanism of DHX9 in human cancers.Frontiers in pharmacology · 2023Article
- The functional impact of BRCA1 BRCT domain variants using multiplexed DNA double-strand break repair assays.American journal of human genetics · 2022Article
- Untangling the crosstalk between BRCA1 and R-loops during DNA repair.Nucleic acids research · 2021Review
- RNA Helicases as Shadow Modulators of Cell Cycle Progression.International journal of molecular sciences · 2021Review
- Article
- The enigmatic helicase DHX9 and its association with the hallmarks of cancer.Future science OA · 2020Review
- IQGAP1 control of centrosome function defines distinct variants of triple negative breast cancer.Oncotarget · 2020Article
- SPOP attenuates migration and invasion of choriocarcinoma cells by promoting DHX9 degradation.American journal of cancer research · 2020Article
- Functional analysis of BARD1 missense variants in homology-directed repair and damage sensitivity.PLoS genetics · 2019Article
- DHX9 inhibits epithelial-mesenchymal transition in human lung adenocarcinoma cells by regulating STAT3.American journal of translational research · 2019Article
- Sei-1 promotes double minute chromosomes formation through activation of the PI3K/Akt/BRCA1-Abraxas pathway and induces double-strand breaks in NIH-3T3 fibroblasts.Cell death & disease · 2018Article
- DHX32 Promotes Angiogenesis in Colorectal Cancer Through Augmenting β-catenin Signaling to Induce Expression of VEGFA.EBioMedicine · 2017Article
- LncRNA AK023948 is a positive regulator of AKT.Nature communications · 2017Article
- DHX32 expression is an indicator of poor breast cancer prognosis.Oncology letters · 2017Article
- RNA helicase DHX9 may be a therapeutic target in lung cancer and inhibited by enoxacin.American journal of translational research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The breast- and ovarian-specific tumor suppressor, BRCA1, has been implicated to function in many nuclear processes, including DNA damage repair, recombination, transcription, ubiquitination, cell cycle checkpoint enforcement, and centrosome regulation. Utilizing a previously described interaction between BRCA1 and RNA helicase A (RHA), we have developed a dominant-negative approach to block BRCA1 function in human breast epithelial cells. Overexpression of a truncated RHA peptide that can bind to the BRCA1 carboxy-terminus prevents normal BRCA1 function, such as BRCA1 association with nuclear foci following DNA damage. Overexpression of this dominant-negative protein induces pleomorphic nuclei, aberrant mitoses with extra centrosomes, and tetraploidy. This model system allows us to observe changes to mammary epithelial cells that occur acutely following loss of BRCA1 function. Furthermore, inhibition of BRCA1 via overexpressing the RHA fragment coincides with a reduction in PARP-1 protein expression, suggesting a possible mechanism for BRCA1 in the maintenance of genomic integrity.
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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.