ArticleOncogene2006
Inhibition of BRCA1 in breast cell lines causes the centrosome duplication cycle to be disconnected from the cell cycle.
Article in Oncogene, 2006. 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
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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, 59 citations in OpenAlex.
- Functional Disruption of IQGAP1 by Truncated PALB2 in Two Cases of Breast Cancer: Implications for Proliferation and Invasion.Biomedicines · 2025Article
- Review
- 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
- BAP1 loss induces mitotic defects in mesothelioma cells through BRCA1-dependent and independent mechanisms.Oncogene · 2023Article
- BRCA1 transports the DNA damage signal for CDDP-induced centrosome amplification through the centrosomal Aurora A.Cancer science · 2022Article
- RAD6 inhibition enhances paclitaxel sensitivity of triple negative breast cancer cells by aggravating mitotic spindle damage.BMC cancer · 2022Article
- Dysregulation of the centrosome induced by BRCA1 deficiency contributes to tissue-specific carcinogenesis.Cancer science · 2021Review
- Review
- IQGAP1 control of centrosome function defines distinct variants of triple negative breast cancer.Oncotarget · 2020Article
- BRCA1 gene: function and deficiency.International journal of clinical oncology · 2018Review
- Aurora A kinase is required for activation of the Fanconi anemia/BRCA pathway upon DNA damage.FEBS open bio · 2016Article
- Centrosomes in the DNA damage response--the hub outside the centre.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016Review
- Rampant centrosome amplification underlies more aggressive disease course of triple negative breast cancers.Oncotarget · 2015Article
- Centrosomal nucleolin is required for microtubule network organization.Cell cycle (Georgetown, Tex.) · 2015Article
- Show me your license, please: deregulation of centriole duplication mechanisms that promote amplification.Cellular and molecular life sciences : CMLS · 2013Review
- KIAA0101 interacts with BRCA1 and regulates centrosome number.Molecular cancer research : MCR · 2011Article
- A clinical overview of centrosome amplification in human cancers.International journal of biological sciences · 2011Review
- Aberrant expression of LMO4 induces centrosome amplification and mitotic spindle abnormalities in breast cancer cells.The Journal of pathology · 2010Article
- Mediator of DNA damage checkpoint 1 (MDC1) regulates mitotic progression.The Journal of biological chemistry · 2009Article
- Regulation of centrosomes by the BRCA1-dependent ubiquitin ligase.Cancer biology & therapy · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
BRCA1-dependent ubiquitination activity regulates centrosome number in several tissue culture cell lines derived from breast cells. In these experiments, we asked how BRCA1 inhibits centrosome amplification. In general, supernumerary centrosomes can accumulate by three mechanisms: (1) failed cytokinesis and the accumulation of centrosomes by duplication in a repeated S-phase of the cell cycle, (2) disruption of the licensing of centrosome doubling such that they duplicate at inappropriate times in the cell cycle, or (3) fragmentation of the centrosomes. In this study, we found that inhibition of BRCA1 caused premature separation of centrioles and reduplication. By blocking cells in early S-phase before centrosome amplification secondary to BRCA1 inhibition could occur and then releasing, we found that inhibition of BRCA1 caused centrosome amplification between late S-phase and G2/M before the cell divided. These results suggest that normal BRCA1 function is critical in these cell lines to prevent centriole separation and centrosome reduplication before mitosis.
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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.