ReviewCytoskeleton (Hoboken, N.J.)2025
PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.
Review in Cytoskeleton (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Combined inhibition of PLK4 and PPM1D promotes cell death in cancer cells with 17q amplification.Cancer cell international · 2026Article
- TRIM37 Expression is Associated with Immune Suppression Poor Response to Neoadjuvant Chemotherapy and Worse Survival in ER-Positive/HER2-Negative Breast Cancer.Annals of surgical oncology · 2026Article
- Visualizing Drosophila centrioles by expansion microscopy.Journal of cell science · 2026Article
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Centrosomes catalyze the assembly of a microtubule-based bipolar spindle, essential for the precise chromosome segregation during cell division. At the center of this process lies Polo-Like Kinase 4 (PLK4), the master regulator that controls the duplication of the centriolar core to ensure the correct balance of two centrosomes per dividing cell. Disruptions in centrosome number or function can lead to genetic disorders such as primary microcephaly or drive tumorigenesis via centrosome amplification. In this context, several chemical inhibitors of PLK4 have emerged as promising therapeutic candidates. The inhibition of PLK4 results in the emergence of acentrosomal cells, which undergo prolonged and error-prone mitosis. This aberrant mitotic duration triggers a "mitotic stopwatch" mechanism that activates the tumor suppressor p53, halting cellular proliferation. However, in a multitude of cancers, the efficacy of this mitotic surveillance mechanism is compromised by mutations that incapacitate p53. Recent investigations have unveiled p53-independent vulnerabilities in cancers characterized by chromosomal gain or amplification of 17q23, which encodes for the ubiquitin ligase TRIM37, in response to PLK4 inhibition, particularly in neuroblastoma and breast cancer. This review encapsulates the latest advancements in our understanding of centriole duplication and acentrosomal cell division in the context of TRIM37 amplification, positioning PLK4 as a compelling target for innovative cancer therapeutics.
Indexed as
Identifiers
What Socratic 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 Socratic graph.