ArticleNature communications2011
Toxicity modelling of Plk1-targeted therapies in genetically engineered mice and cultured primary mammalian cells.
Article in Nature communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 83 citations in OpenAlex.
- Article
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- An In Vivo CRISPR Screen Identifies Stepwise Genetic Dependencies of Metastatic Progression.Cancer research · 2022Article
- The Role of DAPK1 in the Cell Cycle Regulation of Cervical Cancer Cells and in Response to Topotecan.Journal of Cancer · 2022Article
- The Small-Molecule Inhibitor MRIA9 Reveals Novel Insights into the Cell Cycle Roles of SIK2 in Ovarian Cancer Cells.Cancers · 2021Article
- Review
- Targeting pan-essential genes in cancer: Challenges and opportunities.Cancer cell · 2021Review
- Review
- Sarcoma-180 tumor affects the quality of oocytes in mice.Oncology letters · 2021Article
- Phase 1 dose escalation trial of volasertib in combination with decitabine in patients with acute myeloid leukemia.International journal of hematology · 2021Article
- Analyses of expressions and prognostic values of Polo-like kinases in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2020Article
- The Prognostic Relevance of the Proliferation Markers Ki-67 and Plk1 in Early-Stage Ovarian Cancer Patients With Serous, Low-Grade Carcinoma Based on mRNA and Protein Expression.Frontiers in oncology · 2020Article
- Immune adaptor SKAP1 acts a scaffold for Polo-like kinase 1 (PLK1) for the optimal cell cycling of T-cells.Scientific reports · 2019Article
- In vivo rendezvous of small nucleic acid drugs with charge-matched block catiomers to target cancers.Nature communications · 2019Article
- Blocking Mitotic Exit of Ovarian Cancer Cells by Pharmaceutical Inhibition of the Anaphase-Promoting Complex Reduces Chromosomal Instability.Neoplasia (New York, N.Y.) · 2019Article
- Review
- Expression of polo-like kinase 1 in pre-implantation stage murine somatic cell nuclear transfer embryos.Journal of veterinary science · 2019Article
- Polo-like kinases and acute leukemia.Oncogene · 2019Review
- A functional genomics screen reveals a strong synergistic effect between docetaxel and the mitotic gene DLGAP5 that is mediated by the androgen receptor.Cell death & disease · 2018Article
- miR‑23a suppresses pancreatic cancer cell progression by inhibiting PLK‑1 expression.Molecular medicine reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High attrition rates of novel anti-cancer drugs highlight the need for improved models to predict toxicity. Although polo-like kinase 1 (Plk1) inhibitors are attractive candidates for drug development, the role of Plk1 in primary cells remains widely unexplored. Therefore, we evaluated the utility of an RNA interference-based model to assess responses to an inducible knockdown (iKD) of Plk1 in adult mice. Here we show that Plk1 silencing can be achieved in several organs, although adverse events are rare. We compared responses in Plk1-iKD mice with those in primary cells kept under controlled culture conditions. In contrast to the addiction of many cancer cell lines to the non-oncogene Plk1, the primary cells' proliferation, spindle assembly and apoptosis exhibit only a low dependency on Plk1. Responses to Plk1-depletion, both in cultured primary cells and in our iKD-mouse model, correspond well and thus provide the basis for using validated iKD mice in predicting responses to therapeutic interventions.
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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.