ArticleeLife2016
Polo-like kinase 1 induces epithelial-to-mesenchymal transition and promotes epithelial cell motility by activating CRAF/ERK signaling.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Polo-like kinase 1 as a potential therapeutic target and prognostic factor for various human malignancies: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- Targeting Prolyl 3-hydroxylase 1 inhibits pancreatic cancer progression and macrophage immunity.Nature communications · 2026Article
- Multifaceted role of primary cilia and ciliary proteins: A potential nexus for hedgehog signaling and prostate cancer.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Copper modulates cell fate through the PLK1-FOXO3a-β-catenin signaling pathway by differentially regulating cuproptosis and EMT.Apoptosis : an international journal on programmed cell death · 2026Article
- Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026Review
- PLK1 overexpression as a dual-role biomarker and therapeutic vulnerability in pulmonary adenocarcinoma.PeerJ · 2026Article
- Discovery of a novel PLK1 inhibitor with high inhibitory potency using a combined virtual screening strategy.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- The cell cycle regulator PLK1 promotes murine melanoma progression by regulating the transcription factor BACH1.PLoS biology · 2025Article
- Proteins involved in cell division have broad developmental functions.Developmental biology · 2025Article
- Review
- Differential Response and Resistance to KRAS-Targeted Therapy.Molecular carcinogenesis · 2025Review
- MO-2097 inhibits EMT and angiogenesis in colorectal cancer by targeting RAF/MEK/ERK signaling.Scientific reports · 2025Article
- BORA overexpression promotes epithelial-mesenchymal transition and metastasis in ovarian cancer: Unveiling a novel therapeutic target for advanced disease.Clinical and translational medicine · 2025Article
- Onvansertib and Navitoclax Combination as a New Therapeutic Option for Mucinous Ovarian Carcinoma.International journal of molecular sciences · 2025Article
- PLK1 in cancer therapy: a comprehensive review of immunomodulatory mechanisms and therapeutic opportunities.Frontiers in immunology · 2025Review
- The status of p53 affects the efficacy of PLK1 inhibitor BI6727 in prostate cancer cells.Frontiers in cell and developmental biology · 2025Article
- Clinical relevance of PLK1 in epithelial ovarian cancer.Frontiers in pharmacology · 2025Review
- Onvansertib inhibits cell proliferation and increases sensitivity to paclitaxel in uterine serous cancer cells.American journal of cancer research · 2025Article
- TSG6 promotes epithelial-mesenchymal transition and tumor-associated macrophage polarization through Smad2/3 and MAPK signaling by facilitating TSG6-CD44-TGFβR1 or EGFR complex formation.International journal of biological sciences · 2025Article
- Article
20 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Polo-like kinase 1 (PLK1) is a key cell cycle regulator implicated in the development of various cancers, including prostate cancer. However, the functions of PLK1 beyond cell cycle regulation remain poorly characterized. Here, we report that PLK1 overexpression in prostate epithelial cells triggers oncogenic transformation. It also results in dramatic transcriptional reprogramming of the cells, leading to epithelial-to-mesenchymal transition (EMT) and stimulation of cell migration and invasion. Consistently, PLK1 downregulation in metastatic prostate cancer cells enhances epithelial characteristics and inhibits cell motility. The signaling mechanisms underlying the observed cellular effects of PLK1 involve direct PLK1-dependent phosphorylation of CRAF with subsequent stimulation of the MEK1/2-ERK1/2-Fra1-ZEB1/2 signaling pathway. Our findings highlight novel non-canonical functions of PLK1 as a key regulator of EMT and cell motility in normal prostate epithelium and prostate cancer. This study also uncovers a previously unanticipated role of PLK1 as a potent activator of MAPK signaling.
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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.