ArticleScientific reports2017
The responses of cancer cells to PLK1 inhibitors reveal a novel protective role for p53 in maintaining centrosome separation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Polo-like kinase inhibitors increase AAV production by halting cell cycle progression.Molecular therapy. Methods & clinical development · 2025Article
- Targeting Oral Squamous Cell Carcinoma with Combined Polo-Like-Kinase-1 Inhibitors and γ-Radiation Therapy.Biomedicines · 2024Article
- PLK1 inhibitors as a new targeted treatment for adrenocortical carcinoma.Endocrine connections · 2024Article
- Selective protection of normal cells from chemotherapy, while killing drug-resistant cancer cells.Oncotarget · 2023Review
- Virus-like nanoparticles as a theranostic platform for cancer.Frontiers in bioengineering and biotechnology · 2022Review
- Review
- Combinatorial Effect of PLK1 Inhibition with Temozolomide and Radiation in Glioblastoma.Cancers · 2021Article
- Solid tumours hijack the histone variant network.Nature reviews. Cancer · 2021Review
- The Clinical Kinase Index: A Method to Prioritize Understudied Kinases as Drug Targets for the Treatment of Cancer.Cell reports. Medicine · 2020Article
- Analyses of expressions and prognostic values of Polo-like kinases in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2020Article
- Stilbene Compounds Inhibit Tumor Growth by the Induction of Cellular Senescence and the Inhibition of Telomerase Activity.International journal of molecular sciences · 2019Review
- MicroRNA-505 suppresses gastric cancer cell proliferation and invasion by directly targeting Polo-like kinase-1.OncoTargets and therapy · 2019Article
- Polo-like kinase 1 inhibition in NSCLC: mechanism of action and emerging predictive biomarkers.Lung Cancer (Auckland, N.Z.) · 2019Article
- Mutagenic assessment of chemotherapy and Smac mimetic drugs in cells with defective DNA damage response pathways.Scientific reports · 2018Article
- The live cell DNA stain SiR-Hoechst induces DNA damage responses and impairs cell cycle progression.Scientific reports · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Polo-like kinase-1 (PLK1) plays a major role in driving mitotic events, including centrosome disjunction and separation, and is frequently over-expressed in human cancers. PLK1 inhibition is a promising therapeutic strategy and works by arresting cells in mitosis due to monopolar spindles. The p53 tumour suppressor protein is a short-lived transcription factor that can inhibit the growth, or stimulate the death, of developing cancer cells. Curiously, although p53 normally acts in an anti-cancer capacity, it can offer significant protection against inhibitors of PLK1, but the events underpinning this effect are not known. Here, we show that functional p53 reduces the sensitivity to PLK1 inhibitors by permitting centrosome separation to occur, allowing cells to traverse mitosis and re-enter cycle with a normal complement of 2N chromosomes. Protection entails the activation of p53 through the DNA damage-response enzymes, ATM and ATR, and requires the phosphorylation of p53 at the key regulatory site, Ser15. These data highlight a previously unrecognised link between p53, PLK1 and centrosome separation that has therapeutic implications for the use of PLK1 inhibitors in the clinic.
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