ArticlePloS one2010
The Plk1 inhibitor BI 2536 temporarily arrests primary cardiac fibroblasts in mitosis and generates aneuploidy in vitro.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Mass spectrometry-based multi-omics analysis elucidates immune microenvironmental characteristics and the risk of distant metastasis in N1c colorectal cancer.Frontiers in immunology · 2026Article
- Unlocking mitochondrial dysfunction-associated senescence (MiDAS) with NADTranslational oncology · 2024Article
- PLK1 inhibition leads to mitotic arrest and triggers apoptosis in cholangiocarcinoma cells.Oncology letters · 2024Article
- Overexpression of PLK1 relieved the myocardial ischemia-reperfusion injury of rats through inducing the mitophagy and regulating the p-AMPK/FUNDC1 axis.Bioengineered · 2021Article
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- Boolean model of growth signaling, cell cycle and apoptosis predicts the molecular mechanism of aberrant cell cycle progression driven by hyperactive PI3K.PLoS computational biology · 2019Article
- Enhancing Gene-Knockdown Efficiency of Poly(ACS omega · 2018Article
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- Impact of Polo-like kinase 1 inhibitors on human adipose tissue-derived mesenchymal stem cells.Oncotarget · 2016Article
- Therapeutic targeting of polo-like kinase 1 using RNA-interfering nanoparticles (iNOPs) for the treatment of non-small cell lung cancer.Oncotarget · 2015Article
- RNAi screen identifies a synthetic lethal interaction between PIM1 overexpression and PLK1 inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Polo-like kinase-1 in DNA damage response.BMB reports · 2014Review
- Inhibition of Polo kinase by BI2536 affects centriole separation during Drosophila male meiosis.Cell cycle (Georgetown, Tex.) · 2014Article
- AKIP1, a cardiac hypertrophy induced protein that stimulates cardiomyocyte growth via the Akt pathway.International journal of molecular sciences · 2013Article
- Inhibition of polo-like kinase 1 induces cell cycle arrest and sensitizes glioblastoma cells to ionizing radiation.Cancer biotherapy & radiopharmaceuticals · 2013Article
- Battle of the eternal rivals: restoring functional p53 and inhibiting Polo-like kinase 1 as cancer therapy.Oncotarget · 2013Review
- Polo-like kinase 1 inhibitors, mitotic stress and the tumor suppressor p53.Cell cycle (Georgetown, Tex.) · 2013Article
- Antiproliferative in vitro effects of BI 2536-mediated PLK1 inhibition on cervical adenocarcinoma cells.Clinical and experimental medicine · 2013Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BI 2536 is a new anti-mitotic drug that targets polo-like kinase 1 (Plk1) and is currently under clinical development for cancer therapy. The effect of this drug on cancer cells has been extensively investigated, but information about the effects on primary dividing cells and differentiated non-dividing cells is scarce. We have investigated the effects of this drug on primary neonatal rat cardiac fibroblasts and on differentiated cardiomyocytes and explored the possibility to use this drug to enrich differentiated cell populations in vitro. BI 2536 had a profound effect on cardiac fibroblast proliferation in vitro and arrested these cells in mitosis with an IC50 of about 43 nM. Similar results were observed with primary human cells (HUVEC, IC50 = 30 nM), whereas the cancer cell line HeLa was more sensitive (IC50 of 9 nM). Further analysis revealed that prolonged mitotic arrest resulted in cell death for about 40% of cardiac fibroblasts. The remaining cells showed an interphase morphology with mostly multi- and micro-nucleated nuclei. This indicates that a significant number of primary fibroblasts are able to escape BI 2536 induced mitotic arrest and apparently become aneuploid. No effects were observed on cardiomyocytes and hypertrophic response (growth) upon endothelin-1 and phenylephrine stimulation was normal in the presence of BI 2536. This indicates that BI 2536 has no adverse effects on terminally differentiated cells and still allows proliferation independent growth induction in these cells. In conclusion, cardiomyocytes could be enriched using BI 2536, but the formation of aneuploidy in proliferating cells most likely limits this in vitro application and does not allow its use in putative cell based therapies.
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Registered trials
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