ArticleOncogene2009
AKT1 represses gene conversion induced by different genotoxic stresses and induces supernumerary centrosomes and aneuploidy in hamster ovary cells.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Genome rearrangements induced by the stimulation of end-joining of DNA double strand breaks through multiple phosphorylation of MRE11 by the kinase PKB/AKT1.Nucleic acids research · 2025Article
- A Multitarget Gold(I) Complex Induces Cytotoxicity Related to Aneuploidy in HCT-116 Colorectal Carcinoma Cells.Angewandte Chemie (International ed. in English) · 2020Article
- Targeting the PI3K pathway and DNA damage response as a therapeutic strategy in ovarian cancer.Cancer treatment reviews · 2020Review
- Perspective: Potential Impact and Therapeutic Implications of Oncogenic PI3K Activation on Chromosomal Instability.Biomolecules · 2019Review
- Akt1 Stimulates Homologous Recombination Repair of DNA Double-Strand Breaks in a Rad51-Dependent Manner.International journal of molecular sciences · 2017Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- DNA damage response and prostate cancer: defects, regulation and therapeutic implications.Oncogene · 2015Review
- Spontaneous slow replication fork progression elicits mitosis alterations in homologous recombination-deficient mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Is homologous recombination really an error-free process?Frontiers in genetics · 2014Review
- Girdin locates in centrosome and midbody and plays an important role in cell division.Cancer science · 2012Article
- Initiation of DNA double strand break repair: signaling and single-stranded resection dictate the choice between homologous recombination, non-homologous end-joining and alternative end-joining.American journal of cancer research · 2012Article
- Akt: a double-edged sword in cell proliferation and genome stability.Journal of oncology · 2012Article
- Histone methyltransferase EZH2 induces Akt-dependent genomic instability and BRCA1 inhibition in breast cancer.Cancer research · 2011Article
- AKT1/BRCA1 in the control of homologous recombination and genetic stability: the missing link between hereditary and sporadic breast cancers.Oncotarget · 2010Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncogenic kinase AKT1 is frequently overexpressed or activated in sporadic breast and ovarian cancers. In human breast tumors, we have previously shown that AKT1 represses homologous recombination (HR) induced by one double-strand break (DSB). To further analyze the impact of AKT1 on HR, we ectopically expressed wild-type or mutant forms of AKT1 in a hamster ovary cell line containing an intrachromosomal substrate for monitoring HR. In this cell line, AKT1 repressed HR induced by different genotoxic stresses including ionizing radiation, UV-C and one single DSB introduced into the intrachromosomal substrate. Consistently, AKT1 disrupted RAD51 foci formation, showing that AKT1 specifically affects gene conversion. Concomitantly, AKT1 represses both BRCA1 foci formation and HR stimulation resulting from BRCA1 overexpression, showing that AKT1 affects BRCA1-mediated HR functions, also in another species (hamster) and in another type of cell tissue (ovary cells). Finally, consistent with the HR defects, active AKT1 expression induces supernumerary centrosomes and aneuploidy. In addition to its impact on cell proliferation and apoptosis, the present data propose a novel oncogenic function for AKT1, by producing genomic instability as a consequence of HR repression.
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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.