ArticleOncogene2013
p53 modulates homologous recombination at I-SceI-induced double-strand breaks through cell-cycle regulation.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer.International journal of molecular sciences · 2024Review
- Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- Drugging in the absence of p53.Journal of molecular cell biology · 2019Review
- Transcriptional activation of p21Oncotarget · 2018Article
- Targeting Cyclin-Dependent Kinases for Treatment of Gynecologic Cancers.Frontiers in oncology · 2018Review
- Akt1 Stimulates Homologous Recombination Repair of DNA Double-Strand Breaks in a Rad51-Dependent Manner.International journal of molecular sciences · 2017Article
- p53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells.Veterinary research · 2016Article
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- Sensitization of Pancreatic Cancers to Gemcitabine Chemoradiation by WEE1 Kinase Inhibition Depends on Homologous Recombination Repair.Neoplasia (New York, N.Y.) · 2015Article
- Involvement of ATM in homologous recombination after end resection and RAD51 nucleofilament formation.Nucleic acids research · 2015Article
- Increased sensitivity of HPV-positive head and neck cancer cell lines to x-irradiation ± Cisplatin due to decreased expression of E6 and E7 oncoproteins and enhanced apoptosis.American journal of cancer research · 2015Article
- Combined inhibition of Wee1 and PARP1/2 for radiosensitization in pancreatic cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Improving the efficacy of chemoradiation with targeted agents.Cancer discovery · 2014Review
- Article
- Involvement of p53 in the repair of DNA double strand breaks: multifaceted Roles of p53 in homologous recombination repair (HRR) and non-homologous end joining (NHEJ).Sub-cellular biochemistry · 2014Review
- SPOC1 modulates DNA repair by regulating key determinants of chromatin compaction and DNA damage response.Nucleic acids research · 2012Article
- A small RNA response at DNA ends in Drosophila.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of homologous recombination (HR) is believed to be a transactivation-independent function of p53 that protects from genetic instability. Misrepair by HR can lead to genetic alterations such as translocations, duplications, insertions and loss of heterozygosity, which all bear the risk of driving oncogenic transformation. Regulation of HR by wild-type p53 (wtp53) should prevent these genomic rearrangements. Mutation of p53 is a frequent event during carcinogenesis. In particular, dominant-negative mutants inhibiting wtp53 expressed from the unperturbed allel can drive oncogenic transformation by disrupting the p53-dependent anticancer barrier. Here, we asked whether the hot spot mutants R175H and R273H relax HR control in p53-proficient cells. Utilizing an I-SceI-based reporter assay, we observed a moderate (1.5 × ) stimulation of HR upon expression of the mutant proteins in p53-proficient CV-1, but not in p53-deficient H1299 cells. Importantly, the stimulatory effect was exactly paralleled by an increase in the number of HR competent S- and G2-phase cells, which can well explain the enhanced recombination frequencies. Furthermore, the impact on HR exerted by the transactivation domain double-mutant L22Q/W23S and mutant R273P, both of which were reported to regulate HR independently of G1-arrest execution, is also exactly mirrored by cell-cycle behavior. These results are in contrast to previous concepts stating that the transactivation-independent impact of p53 on HR is a general phenomenon valid for replication-associated and also for directly induced double-strand break. Our data strongly suggest that the latter is largely mediated by cell-cycle regulation, a classical transactivation-dependent function of p53.
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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.