ArticleNPJ precision oncology2024
Role of PLK1/NUMB/NOTCH in epithelial-mesenchymal transition in human melanoma.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 7 citations in OpenAlex.
- MZT2A drives epithelial-mesenchymal transition in lung adenocarcinoma via the LGALS3BP/ITGB1/TGF-β/smad2 axis.iScience · 2026Article
- The Trifecta of Polo-Like Kinases, Cancer, and the Immune System: Emerging Intersections and Therapeutic Insights.Molecular cancer research : MCR · 2026Review
- Targeting lysine-specific demethylase 1 inhibits melanoma metastasis via the NF2-Hippo-YAP pathway.Cell death & disease · 2026Article
- A Melanoma-Specific Gene Network Analysis Identifies MZB1 as a Potential Tumor Promoter.The Journal of investigative dermatology · 2026Article
- SIRT6 promotes a mesenchymal, invasive phenotype in melanoma.Journal of dermato-oncology · 2026Article
- S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models.The Journal of clinical investigation · 2025Article
- Polo-like kinase2 regulates renal tubulointerstitial fibrosis via notch signaling pathway in diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Numb and NumbL inhibit melanoma tumor growth by influencing the immune microenvironment.BMC cancer · 2024Article
- Polo-like kinases and UV-induced skin carcinogenesis: What we know and what's next.Photochemistry and photobiologyReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Polo-like kinase 1 (PLK1), a serine/threonine kinase, is overexpressed in melanoma and its expression has been associated with poor disease prognosis. PLK1 has been shown to interact with NUMB, a NOTCH antagonist. However, the exact role of PLK1, NUMB, and NOTCH signaling in epithelial-mesenchymal transition (EMT) in melanoma progression is unclear. In this study, Affymetrix microarray analysis was performed to determine differentially expressed genes following shRNA-mediated knockdown of PLK1 in human melanoma cells that showed significant modulations in EMT and metastasis-related genes. Using multiple PLK1-modulated melanoma cell lines, we found that PLK1 is involved in the regulation of cell migration, invasion, and EMT via its kinase activity and NOTCH activation. In vitro kinase assay and mass spectrometry analysis demonstrated a previously unknown PLK1 phosphorylation site (Ser413) on NUMB. Overexpression of non-phosphorylatable (S413A) and phosphomimetic (S413D) mutants of NUMB in melanoma cells implicated the involvement of NUMB-S413 phosphorylation in cell migration and invasion, which was independent of NOTCH activation. To determine the clinical relevance of these findings, immunohistochemistry was performed using melanoma tissue microarray, which indicated a strong positive correlation between PLK1 and N-cadherin, a protein required for successful EMT. These findings were supported by TCGA analysis, where expression of high PLK1 with low NUMB or high NOTCH or N-cadherin showed a significant decrease in survival of melanoma patients. Overall, these results suggest a potential role of PLK1 in EMT, migration, and invasion of melanoma cells. Our findings support the therapeutic targeting of PLK1, NUMB, and NOTCH for melanoma management.
Identifiers
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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.