ArticleCell cycle (Georgetown, Tex.)2013
Polo-like kinase 1 inhibitors, mitotic stress and the tumor suppressor p53.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- The status of p53 affects the efficacy of PLK1 inhibitor BI6727 in prostate cancer cells.Frontiers in cell and developmental biology · 2025Article
- Involvement of RBP-J interacting and tubulin-associated protein in the distribution of protein regulator of cytokinesis 1 in mitotic spindles.Frontiers in cell and developmental biology · 2024Article
- Target Analysis and Mechanism of Podophyllotoxin in the Treatment of Triple-Negative Breast Cancer.Frontiers in pharmacology · 2020Article
- Non-canonical cMet regulation by vimentin mediates Plk1 inhibitor-induced apoptosis.EMBO molecular medicine · 2019Article
- In vitro study of the Polo-like kinase 1 inhibitor volasertib in non-small-cell lung cancer reveals a role for the tumor suppressor p53.Molecular oncology · 2019Article
- The responses of cancer cells to PLK1 inhibitors reveal a novel protective role for p53 in maintaining centrosome separation.Scientific reports · 2017Article
- Deficiency of RITA results in multiple mitotic defects by affecting microtubule dynamics.Oncogene · 2017Article
- Aberrant DNA Double-strand Break Repair Threads in Breast Carcinoma: Orchestrating Genomic Insult Survival.Journal of cancer prevention · 2016Review
- B-cell lymphoma 6 promotes proliferation and survival of trophoblastic cells.Cell cycle (Georgetown, Tex.) · 2016Article
- Combining p53 stabilizers with metformin induces synergistic apoptosis through regulation of energy metabolism in castration-resistant prostate cancer.Cell cycle (Georgetown, Tex.) · 2016Article
- Adenovirus replaces mitotic checkpoint controls.Journal of virology · 2015Article
- The activity regulation of the mitotic centromere-associated kinesin by Polo-like kinase 1.Oncotarget · 2015Article
- Loss of p21Cip1/CDKN1A renders cancer cells susceptible to Polo-like kinase 1 inhibition.Oncotarget · 2015Article
- Article
- Functional analysis of phosphorylation of the mitotic centromere-associated kinesin by Aurora B kinase in human tumor cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Phase I study of oral rigosertib (ON 01910.Na), a dual inhibitor of the PI3K and Plk1 pathways, in adult patients with advanced solid malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Remote loading of preencapsulated drugs into stealth liposomes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Polo-like kinase 1 inhibition causes decreased proliferation by cell cycle arrest, leading to cell death in glioblastoma.Cancer gene therapy · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinase 1 has been established as one of the most attractive targets for molecular cancer therapy. In fact, multiple small-molecule inhibitors targeting this kinase have been developed and intensively investigated. Recently, it has been reported that the cytotoxicity induced by Plk1 inhibition is elevated in cancer cells with inactive p53, leading to the hypothesis that inactive p53 is a predictive marker for the response of Plk1 inhibition. In our previous study based on different cancer cell lines, we showed that cancer cells with wild type p53 were more sensitive to Plk1 inhibition by inducing more apoptosis, compared with cancer cells depleted of p53. In the present work, we further demonstrate that in the presence of mitotic stress induced by different agents, Plk1 inhibitors strongly induced apoptosis in HCT116 p53(+/+) cells, whereas HCT116 p53(-/-) cells arrested in mitosis with less apoptosis. Depletion of p53 in HCT116 p53(+/+) or U2OS cells reduced the induction of apoptosis. Moreover, the surviving HCT116 p53(-/-) cells showed DNA damage and a strong capability of colony formation. Plk1 inhibition in combination with other anti-mitotic agents inhibited proliferation of tumor cells more strongly than Plk1 inhibition alone. Taken together, the data underscore that functional p53 strengthens the efficacy of Plk1 inhibition alone or in combination by strongly activating cell death signaling pathways. Further studies are required to investigate if the long-term outcomes of losing p53, such as low differential grade of tumor cells or defective DNA damage checkpoint, are responsible for the cytotoxicity of Plk1 inhibition.
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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.