ArticleOncogene2017
Inhibition of Polo-like kinase 1 during the DNA damage response is mediated through loss of Aurora A recruitment by Bora.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- Cell cycle oscillations in a polarity network facilitate state switching by morphogenetic cues.Science advances · 2026Article
- Molecular basis for the activation of Aurora A and Plk1 kinases during mitotic entry.The EMBO journal · 2026Article
- Cell cycle oscillations in a polarity network facilitate state switching by morphogenetic cues.bioRxiv : the preprint server for biology · 2025Article
- A deep single cell mass cytometry approach to capture canonical and noncanonical cell cycle states.Nature communications · 2025Article
- BRCA1 orchestrates the response to BI-2536 and its combination with alisertib in MYC-driven small cell lung cancer.Cell death & disease · 2024Article
- Targeting Oral Squamous Cell Carcinoma with Combined Polo-Like-Kinase-1 Inhibitors and γ-Radiation Therapy.Biomedicines · 2024Article
- Emerging roles of Aurora-A kinase in cancer therapy resistance.Acta pharmaceutica Sinica. B · 2023Review
- Targeting lysine-specific demethylase 1 (KDM1A/LSD1) impairs colorectal cancer tumorigenesis by affecting cancer cells stemness, motility, and differentiation.Cell death discovery · 2023Article
- CDC6 as a Key Inhibitory Regulator of CDK1 Activation Dynamics and the Timing of Mitotic Entry and Progression.Biology · 2023Review
- PARP1 and CHK1 coordinate PLK1 enzymatic activity during the DNA damage response to promote homologous recombination-mediated repair.Nucleic acids research · 2021Article
- In search for biomarkers and potential drug targets for uterine serous endometrial cancer.Journal of cancer research and clinical oncology · 2021Article
- Dysregulated G2 phase checkpoint recovery pathway reduces DNA repair efficiency and increases chromosomal instability in a wide range of tumours.Oncogenesis · 2021Article
- Investigating Molecular Determinants of Cancer Cell Resistance to Ionizing Radiation Through an Integrative Bioinformatics Approach.Frontiers in cell and developmental biology · 2021Article
- The CINs of Polo-Like Kinase 1 in Cancer.Cancers · 2020Review
- A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.Cell cycle (Georgetown, Tex.) · 2020Review
- Quantitative phosphoproteomics to unravel the cellular response to chemical stressors with different modes of action.Archives of toxicology · 2020Article
- Review
- BORA regulates cell proliferation and migration in bladder cancer.Cancer cell international · 2020Article
- DNA replication and mitotic entry: A brake model for cell cycle progression.The Journal of cell biology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When cells in G2 phase are challenged with DNA damage, several key mitotic regulators such as Cdk1/Cyclin B, Aurora A and Plk1 are inhibited to prevent entry into mitosis. Here we have studied how inhibition of Plk1 is established after DNA damage. Using a Förster resonance energy transfer (FRET)-based biosensor for Plk1 activity, we show that inhibition of Plk1 after DNA damage occurs with relatively slow kinetics and is entirely dependent on loss of Plk1-T210 phosphorylation. As T210 is phosphorylated by the kinase Aurora A in conjunction with its co-factor Bora, we investigated how they are affected by DNA damage. Interestingly, we find that the interaction between Bora and Plk1 remains intact during the early phases of the DNA damage response (DDR), whereas Plk1 activity is already inhibited at this stage. Expression of an Aurora A mutant that is refractory to inhibition by the DDR failed to prevent inhibition of Plk1 and loss of T210 phosphorylation, suggesting that inhibition of Plk1 may be established by perturbing recruitment of Aurora A by Bora. Indeed, expression of a fusion in which Aurora A was directly coupled to Bora prevented DNA damage-induced inhibition of Plk1 activity, as well as inhibition of T210 phosphorylation. Taken together, these data demonstrate that DNA damage affects the function of Aurora A at multiple levels: both by direct inhibition of Aurora A activity, as well as by perturbing the interaction with its co-activator Bora. We propose that the DDR targets recruitment of Aurora A to the Plk1/Bora complex to prevent activation of Plk1 during DNA damage in G2.
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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.