ArticleOncogene2004
Genotoxic stress leads to centrosome amplification in breast cancer cell lines that have an inactive G1/S cell cycle checkpoint.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 70 citations in OpenAlex.
- Centriolar satellites regulateMolecular biology of the cell · 2026Article
- Centriolar satellites regulatebioRxiv : the preprint server for biology · 2026Article
- 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
- Epigenetic alterations impede epithelial-mesenchymal transition by modulating centrosome amplification and Myc/RAS axis in triple negative breast cancer cells.Scientific reports · 2023Article
- Inhibition of triple‑negative breast cancer proliferation and motility by reactivating p53 and inhibiting overactivated Akt.Oncology reports · 2022Article
- MASTL: A novel therapeutic target for Cancer Malignancy.Cancer medicine · 2020Review
- G2/M inhibitors as pharmacotherapeutic opportunities for glioblastoma: the old, the new, and the future.Cancer biology & medicine · 2018Article
- Aurora-A overexpression is linked to development of aggressive teratomas derived from human iPS cells.Oncology reports · 2018Article
- A linear programming computational framework integrates phosphor-proteomics and prior knowledge to predict drug efficacy.BMC systems biology · 2017Article
- Molecular targeting of the Aurora-A/SMAD5 oncogenic axis restores chemosensitivity in human breast cancer cells.Oncotarget · 2017Article
- Centrosome amplification: a suspect in breast cancer and racial disparities.Endocrine-related cancer · 2017Review
- Centrosome amplification, chromosomal instability and cancer: mechanistic, clinical and therapeutic issues.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016Review
- Aurora-A Kinase as a Promising Therapeutic Target in Cancer.Frontiers in oncology · 2015Review
- Inhibition of Cdk2 kinase activity selectively targets the CD44⁺/CD24⁻/Low stem-like subpopulation and restores chemosensitivity of SUM149PT triple-negative breast cancer cells.International journal of oncology · 2014Article
- Quantitative multi-parametric evaluation of centrosome declustering drugs: centrosome amplification, mitotic phenotype, cell cycle and death.Cell death & disease · 2014Article
- Genotoxicity of multi-walled carbon nanotubes at occupationally relevant doses.Particle and fibre toxicology · 2014Article
- Article
- Inhibition of Cdk2 activity decreases Aurora-A kinase centrosomal localization and prevents centrosome amplification in breast cancer cells.Oncology reports · 2013Article
- Show me your license, please: deregulation of centriole duplication mechanisms that promote amplification.Cellular and molecular life sciences : CMLS · 2013Review
- Cdk4 and nek2 signal binucleation and centrosome amplification in a her2+ breast cancer model.PloS one · 2013Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Centrosome amplification plays a key role in the origin of chromosomal instability during cancer development and progression. In this study, breast cancer cell lines with different p53 backgrounds were used to investigate the relationship between genotoxic stress, G(1)/S cell cycle checkpoint integrity, and the development of centrosome amplification. Introduction of DNA damage in the MCF-7 cell line by treatment with hydroxyurea (HU) or daunorubicin (DR) resulted in the arrest of both G(1)/S cell cycle progression and centriole duplication. In these cells, which carry functional p53, HU treatment also led to nuclear accumulation of p53 and p21(WAF1), retinoblastoma hypophosphorylation, and downregulation of cyclin A. MCF-7 cells carrying a recombinant dominant-negative p53 mutant (vMCF-7(DNp53)) exhibited a shortened G(1) phase of the cell cycle and retained a normal centrosome phenotype. However, these cells developed amplified centrosomes following HU treatment. The MDA-MB 231 cell line, which carries mutant p53 at both alleles, showed amplified centrosomes at the outset, and developed a hyperamplified centrosome phenotype following HU treatment. In cells carrying defective p53, the development of centrosome amplification also occurred following treatment with another DNA damaging agent, DR. Taken together, these findings demonstrate that loss of p53 function alone is not sufficient to drive centrosome amplification, but plays a critical role in this process following DNA damage through abrogation of the G(1)/S cell cycle checkpoint. Furthermore, these studies have important clinical implications because they suggest that breast cancers with compromised p53 function may develop centrosome amplification and consequent chromosomal instability following treatment with genotoxic anticancer drugs.
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