ArticleOncotarget2015
Mitotic entry: Non-genetic heterogeneity exposes the requirement for Plk1.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular basis for the activation of Aurora A and Plk1 kinases during mitotic entry.The EMBO journal · 2026Article
- Mitotic entry upon Topo II catalytic inhibition is controlled by Chk1 and Plk1.The FEBS journal · 2020Article
- Oncogenic MYC amplifies mitotic perturbations.Open biology · 2019Article
- Phosphatidylinositol-5-phosphate 4-kinase gamma accumulates at the spindle pole and prevents microtubule depolymerization.Cell division · 2019Article
- A unified view of spatio-temporal control of mitotic entry: Polo kinase as the key.Open biology · 2018Review
- Dialogue between centrosomal entrance and exit scaffold pathways regulates mitotic commitment.The Journal of cell biology · 2017Article
- Re-investigating PLK1 inhibitors as antimitotic agents.Molecular & cellular oncology · 2017Article
- Modeling Cancer Cell Growth DynamicsFrontiers in oncology · 2017Article
- Inhibition of Bcl-xL sensitizes cells to mitotic blockers, but not mitotic drivers.Open biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The quest to develop novel antimitotic chemotherapy agents has led to the generation of several small molecule inhibitors targeting Plk1, a protein kinase required for multiple aspects of cell division. Previous studies have shown that upon exposure to Plk1 inhibitors, cells enter mitosis, delay briefly in prophase and then arrest in mitosis due to an inability to undergo centrosome separation. Here, we show that four different classes of Plk1 inhibitor block mitotic entry in several cancer cell lines and non-transformed RPE-1 cells. The proportion of cells that arrest in G2 is cell line and concentration dependent, and is subject to non-genetic heterogeneity. Following inhibitor washout, the G2 block is alleviated and cells enter mitosis but then fail to complete cell division indicating that most Plk1 inhibitors are not fully reversible. An exception is CYC140844; in contrast to five other inhibitors examined here, this novel Plk1 inhibitor is fully reversible. We discuss the implications for developing Plk1 inhibitors as chemotherapy agents and research tools.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.