ArticleCell cycle (Georgetown, Tex.)2015
Functional relationship among PLK2, PLK4 and ROCK2 to induce centrosome amplification.
Article in Cell cycle (Georgetown, Tex.), 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
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
- Polo-Like Kinase 2: From Principle to Practice.Frontiers in oncology · 2022Review
- Biological and clinical significance of flap endonuclease‑1 in triple‑negative breast cancer: Support of metastasis and a poor prognosis.Oncology reports · 2020Article
- RhoC regulates radioresistance via crosstalk of ROCK2 with the DNA repair machinery in cervical cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- POLQ Overexpression Is Associated with an Increased Somatic Mutation Load and PLK4 Overexpression in Lung Adenocarcinoma.Cancers · 2019Article
- Histone Deacetylase SIRT1 Targets Plk2 to Regulate Centriole Duplication.Cell reports · 2018Article
- High LIN28A and PLK4 co‑expression is associated with poor prognosis in epithelial ovarian cancer.Molecular medicine reports · 2018Article
- 14-3-3γ Prevents Centrosome Amplification and Neoplastic Progression.Scientific reports · 2016Article
- Cytoplasmic nucleophosmin has elevated T199 phosphorylation upon which G2/M phase progression is dependent.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The presence of more than 2 centrosomes (centrosome amplification) leads to defective mitosis and chromosome segregation errors, is frequently found in a variety of cancer types, and believed to be the major cause of chromosome instability. One mechanism for generation of amplified centrosomes is over-duplication of centrosomes in a single cell cycle, which is expected to occur when cells are temporarily arrested. There are a growing number of kinases that are critical for induction and promotion of centrosome amplification in the cell cycle-arrested cells, including Rho-associated kinase (ROCK2), Polo-like kinase 2 (PLK2) and PLK4. Here, we tested whether these kinases induce centrosome amplification in a linear pathway or parallel pathways. We first confirmed that ROCK2, PLK2 and PLK4 are all essential for centrosomes to re-duplicate in the cells arrested by exposure to DNA synthesis inhibitor. Using the centrosome amplification rescue assay, we found that PLK2 indirectly activates ROCK2 via phosphorylating nucleophosmin (NPM), and PLK4 functions downstream of ROCK2 to drive centrosome amplification in the arrested cells.
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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.