ReviewOncogene2016
The role of Plk3 in oncogenesis.
Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 91 citations in OpenAlex.
- Article
- Insights into Molecular Mechanisms of Polyphenolic Compounds fromPharmaceuticals (Basel, Switzerland) · 2026Article
- New Insights Into the Role of Polo-Like Kinase 3 in Lung Tumorigenesis.Journal of cellular biochemistry · 2026Article
- Decoding cross-talk between Mpox and HIV: insights from transcriptomics and network-based analyses.Virology journal · 2025Article
- PLK3 weakens antioxidant defense and inhibits proliferation of porcine Leydig cells under oxidative stress.Scientific reports · 2025Article
- Integrated machine learning survival framework to decipher diverse cell death patterns for predicting prognosis in lung adenocarcinoma.Genes and immunity · 2024Article
- Article
- The prognostic values and immune characteristics of polo-like kinases (PLKs) family: A pan-cancer multi-omics analysis.Heliyon · 2024Article
- Nardilysin-regulated scission mechanism activates polo-like kinase 3 to suppress the development of pancreatic cancer.Nature communications · 2024Article
- LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling.Molecular cancer · 2024Article
- The oncogenic mechanisms of the Janus kinase-signal transducer and activator of transcription pathway in digestive tract tumors.Cell communication and signaling : CCS · 2024Review
- An orchestra of machine learning methods reveals landmarks in single-cell data exemplified with aging fibroblasts.PloS one · 2024Article
- ALDH1A1 drives prostate cancer metastases and radioresistance by interplay with AR- and RAR-dependent transcription.Theranostics · 2024Article
- High PLK3 levels are linked with less tumor invasion, lower FIGO stage and better prognosis of endometrial cancer.Biomarkers in medicine · 2024Article
- PLK3 is linked with higher tumor stage and unfavorable prognosis in patients with colorectal cancer.Biomarkers in medicine · 2024Article
- PLK3 facilitates replication of swine influenza virus by phosphorylating viral NP protein.Emerging microbes & infections · 2023Article
- PLK3 promotes the proneural-mesenchymal transition in glioblastoma via transcriptional regulation of C5AR1.Molecular biology reports · 2023Article
- Article
- Development of Cell Permeable NanoBRET Probes for the Measurement of PLK1 Target Engagement in Live Cells.Molecules (Basel, Switzerland) · 2023Article
- Development of Cell Permeable NanoBRET Probes for the Measurement of PLK1 Target Engagement in Live Cells.bioRxiv : the preprint server for biology · 2023Article
4 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polo-like kinases (Plks) encompass a family of five serine/threonine protein kinases that play essential roles in many cellular processes involved in the control of the cell cycle, including entry into mitosis, DNA replication and the response to different types of stress. Plk1, which has been validated as a cancer target, came into the focus of many pharmaceutical companies for the development of small-molecule inhibitors as anticancer agents. Recently, FDA (Food and Drug Administration) has granted a breakthrough therapy designation to the Plk inhibitor BI 6727 (volasertib), which provided a survival benefit for patients suffering from acute myeloid leukemia. However, the various ATP-competitive inhibitors of Plk1 that are currently in clinical development also inhibit the activities of Plk2 and Plk3, which are considered as tumor suppressors. Plk3 contributes to the control and progression of the cell cycle while acting as a mediator of apoptosis and various types of cellular stress. The aberrant expression of Plk3 was found in different types of tumors. Recent progress has improved our understanding of Plk3 in regulating stress signaling and tumorigenesis. When using ATP-competitive Plk1 inhibitors, the biological roles of Plk1-related family members like Plk3 in cancer cells need to be considered carefully to improve treatment strategies against cancer.
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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.