ArticleThe Journal of biological chemistry2007
The Wnt5A/protein kinase C pathway mediates motility in melanoma cells via the inhibition of metastasis suppressors and initiation of an epithelial to mesenchymal transition.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers.
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Who cites it
202 citing papers in PubMed, 366 citations in OpenAlex.
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Role of the Wnt5A pathway in resistance to immune checkpoint inhibitors in advanced Non-Small Cell Lung Cancer.Cancer immunology, immunotherapy : CII · 2026Article
- Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Harnessing Next-Generation 3D Cancer Models to Elucidate Tumor-Microbiome Crosstalk.Advanced healthcare materials · 2026Review
- Effects of SOX10 on the proliferative, invasive, migratory, and epithelial-mesenchymal transition abilities of triple-negative breast cancer cells.Frontiers in oncology · 2026Article
- Conditional deletion ofFrontiers in cell and developmental biology · 2026Article
- SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells.NAR cancer · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- The role of ESRP1 in solid tumor development through the regulation of CD44 splicing and EMT processes.Frontiers in oncology · 2025Review
- Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.Current cardiology reviews · 2025Review
- Wnt Signaling Pathway in Tumor Biology.Genes · 2024Review
- Expression ofCells · 2024Article
- Review
- Mitotic Spindle Positioning (MISP) Facilitates Colorectal Cancer Progression by Forming a Complex with Opa Interacting Protein 5 (OIP5) and Activating the JAK2-STAT3 Signaling Pathway.International journal of molecular sciences · 2024Article
- miR-139-3p/Wnt5A Axis Inhibits Metastasis in Hepatoblastoma.Molecular biotechnology · 2023Article
- Therapeutic targeting approach on epithelial-mesenchymal plasticity to combat cancer metastasis.Medical oncology (Northwood, London, England) · 2023Review
- Olfactomedin 4 produces dysplasia but suppresses metastasis of colon cancer.Cancer gene therapy · 2023Article
- Noncanonical Wnt signaling promotes colon tumor growth, chemoresistance and tumor fibroblast activation.EMBO reports · 2023Article
- Phenotype Switching and the Melanoma Microenvironment; Impact on Immunotherapy and Drug Resistance.International journal of molecular sciences · 2023Review
- Article
142 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
We have shown that Wnt5A increases the motility of melanoma cells. To explore cellular pathways involving Wnt5A, we compared gain-of-function (WNT5A stable transfectants) versus loss-of-function (siRNA knockdown) of WNT5A by microarray analysis. Increasing WNT5A suppressed the expression of several genes, which were re-expressed after small interference RNA-mediated knockdown of WNT5A. Genes affected by WNT5A include KISS-1, a metastasis suppressor, and CD44, involved in tumor cell homing during metastasis. This could be validated at the protein level using both small interference RNA and recombinant Wnt5A (rWnt5A). Among the genes up-regulated by WNT5A was the gene vimentin, associated with an epithelial to mesenchymal transition (EMT), which involves decreases in E-cadherin, due to up-regulation of the transcriptional repressor, Snail. rWnt5A treatment increases Snail and vimentin expression, and decreases E-cadherin, even in the presence of dominant-negativeTCF4, suggesting that this activation is independent of Wnt/beta-catenin signaling. Because Wnt5A can signal via protein kinase C (PKC), the role of PKC in Wnt5A-mediated motility and EMT was also assessed using PKC inhibition and activation studies. Treating cells expressing low levels of Wnt5A with phorbol ester increased Snail expression inhibiting PKC in cells expressing high levels of Wnt5A decreased Snail. Furthermore, inhibition of PKC before Wnt5A treatment blocked Snail expression, implying that Wnt5A can potentiate melanoma metastasis via the induction of EMT in a PKC-dependent manner.
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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.