ArticleInternational journal of oncology2019
High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
- Design, Synthesis, and Biological Activity Evaluation of Quinazoline-Based PLK4 Inhibitors.Biomedicines · 2026Article
- Polo-like kinase 5 is lowly expressed and negatively correlates with poorer differentiation, and its positivity may predict a better prognosis in patients with colorectal cancer.Discover oncology · 2026Article
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- Review
- M phase-specific generation of supernumerary centrioles in cancer cells.Molecular biology of the cell · 2025Article
- Developmental and tissue-specific roles of mammalian centrosomes.The FEBS journal · 2025Review
- Prolonged overexpression of PLK4 leads to formation of centriole rosette clusters that are connected via canonical centrosome linker proteins.Scientific reports · 2024Article
- Tumor polo-like kinase 4 protein expression reflects lymphovascular invasion, higher Federation of Gynecology and Obstetrics stage, and shortened survival in endometrial cancer patients who undergo surgical resection.BMC women's health · 2024Article
- Role of non-coding RNAs in neuroblastoma.Cancer gene therapy · 2023Review
- Expanding roles of centrosome abnormalities in cancers.BMB reports · 2023Review
- Polo-like kinase 4 (Plk4) potentiates anoikis-resistance of p53KO mammary epithelial cells by inducing a hybrid EMT phenotype.Cell death & disease · 2023Article
- Centrosomal protein 120 promotes centrosome amplification and gastric cancer progression via USP54-mediated deubiquitination of PLK4.iScience · 2023Article
- Aberrant expression of polo-like kinase 4 in renal cell carcinoma: Association with clinicopathological characteristics and long-term survival.Oncology letters · 2022Article
- Polo-like kinase 4 is associated with advanced TNM stages and reduced survival and its inhibition improves chemosensitivity in colorectal cancer.Oncology letters · 2022Article
- Downregulation of PLK4 expression induces apoptosis and G0/G1-phase cell cycle arrest in keloid fibroblasts.Cell proliferation · 2022Article
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- Article
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Identification of 9 Gene Signatures by WGCNA to Predict Prognosis for Colon Adenocarcinoma.Computational intelligence and neuroscience · 2022Article
- Role of Hub Genes in the Occurrence and Development of Testicular Cancer Based on Bioinformatics.International journal of general medicine · 2022Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo‑like kinase 4 (PLK4) has been identified as an oncogene, which is overexpressed in various types of human cancer; however, its role in colorectal cancer (CRC) development remains unknown. The present study demonstrated that PLK4 protein expression was upregulated in CRC tissues compared with in normal tissues through western blotting. In addition, immunohistochemical analysis of 39 CRC specimens further demonstrated that PLK4 protein expression was upregulated in 64.1% (25/39) of samples. Increased PLK4 expression was closely associated with enhanced tumor size (P=0.031), lymph node metastasis (P=0.016) and TNM stage (P=0.001). Subsequently, cell viability, wound scratch, migration and invasion assays were conducted in vitro, and nude mice CRC xenograft models were generated. The results demonstrated that knockdown of PLK4 in CRC cells resulted in significant decreases in cell viability and proliferation, and decreased the protein expression levels of N‑cadherin and snail, which are biomarkers of epithelial‑mesenchymal transition. Furthermore, PLK4 knockdown inactivated the Wnt/β‑catenin pathway in CRC cells in vitro and in vivo, and suppressed the growth of xenograft tumors in nude mice. In conclusion, these results suggested that PLK4 may promote the carcinogenesis and metastasis of CRC, thus indicating that PLK4 may be considered a molecular target for CRC treatment.
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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.