ArticleOncology reports2019
Polo‑like kinase 4 promotes tumorigenesis and induces resistance to radiotherapy in glioblastoma.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 28 citations in OpenAlex.
- Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Druggable target ATAD2 enhances the malignant progression and cooperates with E2F1 to up-regulate PDK1 expression in glioma.Genes & diseases · 2026Article
- Review
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- ATAD2 as a Cancer Target: Insights into Its Structure, Functions, Mechanisms, and Drug Development.Cancers · 2025Review
- Unveiling the significance of cancer-testis antigens and their implications for immunotherapy in glioma.Discover oncology · 2024Review
- Spermatocytes have the capacity to segregate chromosomes despite centriole duplication failure.EMBO reports · 2024Article
- CRISPR screens reveal convergent targeting strategies against evolutionarily distinct chemoresistance in cancer.Nature communications · 2024Article
- Role of non-coding RNAs in neuroblastoma.Cancer gene therapy · 2023Review
- Polo-like kinase 4 is associated with advanced TNM stages and reduced survival and its inhibition improves chemosensitivity in colorectal cancer.Oncology letters · 2022Article
- Tumor-Promoting ATAD2 and Its Preclinical Challenges.Biomolecules · 2022Review
- Article
- Polo-like kinase 4 as a potential predictive biomarker of chemoradioresistance in locally advanced rectal cancer.Journal of pathology and translational medicine · 2022Article
- Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer.FEBS open bio · 2021Article
- Identification and assessment of PLK1/2/3/4 in lung adenocarcinoma and lung squamous cell carcinoma: Evidence from methylation profile.Journal of cellular and molecular medicine · 2021Article
- CircKIF2A contributes to cell proliferation, migration, invasion and glycolysis in human neuroblastoma by regulating miR-129-5p/PLK4 axis.Molecular and cellular biochemistry · 2021Article
- Review
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- Polo-like kinase 4 correlates with greater tumor size, lymph node metastasis and confers poor survival in non-small cell lung cancer.Journal of clinical laboratory analysis · 2020Article
- Targeting bromodomain protein ANCCA/ATAD2 enhances the efficacy of DNA‑damaging chemotherapy agents and radiation.Oncology reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is one of the most malignant tumors in adults, associated with severe outcomes (median survival, <2 years). Multiple mechanisms are known to be involved in tumor recurrence and treatment resistance in GBM, however, the key regulator for GBM tumorigenesis and therapy resistance remains unclear. To clarify a novel potential functional mechanism of GBM recurrence, a wide range of experiments including in vitro molecular biological experiments and in vivo intracranial xenograft tumor models were performed in the present study. With bioinformatics analysis, polo‑like kinase 4 (PLK4) was initially identified as one of the most upregulated kinase encoding genes in GBM, which was functionally required for both in vitro cell proliferation and in vivo tumorigenesis in GBM. Clinically, an elevated PLK4 expression was observed in high grade glioma patients, which was associated with poor prognosis. In addition, PLK4 enhanced radioresistance in GBM, while PLK4 knockdown via lentivirus transfection significantly increased the radiosensitivity of GBM cells. Mechanically, PLK4 expression was markedly elevated by the exogenous overexpression of ATPase family AAA domain‑containing protein 2 (ATAD2) in GBM cells. Collectively, the results suggested that the ATAD2‑dependent transcriptional regulation of PLK4 promoted cell proliferation and tumorigenesis, as well as radioresistance in GBM, thus potentially inducing tumor recurrence. PLK4 could therefore serve as a potential therapeutic target for GBM treatment.
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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.