ArticlePloS one2013
N-cadherin dependent collective cell invasion of prostate cancer cells is regulated by the N-terminus of α-catenin.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- Desmocollin-3 Is a Novel Target Receptor for Targeted Drug Delivery for Malignant Prostate Cancer.Pharmaceutics · 2026Article
- ATGL-mediated lipid droplet lipolysis promotes collective migration in Drosophila.bioRxiv : the preprint server for biology · 2026Article
- Cytokines IL-6, IL-10, and CCL5 Secreted by Infiltrating B Cells Promote Cell Migration of Human Prostate Cancer Cell Lines.Oncology research · 2026Article
- Homotypic Targeting of [Pharmaceutics · 2025Article
- 4D pathology: translating dynamic epithelial tubulogenesis to prostate cancer pathology.Histopathology · 2025Review
- Navigating the Collective: Nanoparticle-Assisted Identification of Leader Cancer Cells During Migration.Life (Basel, Switzerland) · 2025Article
- Liver X Receptors Enhance Epithelial to Mesenchymal Transition in Metastatic Prostate Cancer Cells.Cancers · 2024Article
- Alternative molecular mechanisms for force transmission at adherens junctions via β-catenin-vinculin interaction.Nature communications · 2024Article
- Extracellular Mechanical Stimuli Alters the Metastatic Progression of Prostate Cancer Cells within 3D Tissue Matrix.Bioengineering (Basel, Switzerland) · 2023Article
- Pacsin 2-dependent N-cadherin internalization regulates the migration behaviour of malignant cancer cells.Journal of cell science · 2023Article
- Article
- Prostate cancer bone metastases biology and clinical management (Review).Oncology letters · 2023Review
- The metastatic capacity of high-grade serous ovarian cancer cells changes along disease progression: inhibition by mifepristone.Cancer cell international · 2022Article
- Prostate cancer cells of increasing metastatic potential exhibit diverse contractile forces, cell stiffness, and motility in a microenvironment stiffness-dependent manner.Frontiers in cell and developmental biology · 2022Article
- BACH1 promotes the progression of esophageal squamous cell carcinoma by inducing the epithelial-mesenchymal transition and angiogenesis.Cancer medicine · 2021Article
- The role of N-cadherin/c-Jun/NDRG1 axis in the progression of prostate cancer.International journal of biological sciences · 2021Article
- Specific Binding of Novel SPION-Based System Bearing Anti-N-Cadherin Antibodies to Prostate Tumor Cells.International journal of nanomedicine · 2021Article
- Hypoxia, partial EMT and collective migration: Emerging culprits in metastasis.Translational oncology · 2020Review
- MicroRNA-195 inhibits proliferation and metastasis in renal cell carcinoma via regulating HMGA1.American journal of translational research · 2020Article
- Netrin-1 promotes the collective cell migration of liver cancer cells in a 3D cell culture model.Journal of physiology and biochemistry · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cell invasion is the critical first step of metastasis, yet, little is known about how cancer cells invade and initiate metastasis in a complex extracellular matrix. Using a cell line from bone metastasis of prostate cancer (PC3), we analyzed how prostate cancer cells migrate in a physiologically relevant 3D Matrigel. We found that PC3 cells migrated more efficiently as multi-cellular clusters than isolated single cells, suggesting that the presence of cell-cell adhesion improves 3D cell migration. Perturbation of N-cadherin function by transfection of either the N-cadherin cytoplasmic domain or shRNA specific to N-cadherin abolished collective cell migration. Interestingly, PC3 cells do not express α-catenin, an actin binding protein in the cadherin complex. When the full-length α-catenin was re-introduced, the phenotype of PC3 cells reverted back to a more epithelial phenotype with a decreased cell migration rate in 3D Matrigel. Interestingly, we found that the N-terminal half of α-catenin was sufficient to suppress invasive phenotype. Taken together, these data suggest that the formation of N-cadherin junctions promotes 3D cell migration of prostate cancer cells, and this is partly due to an aberrant regulation of the N-cadherin complex in the absence of α-catenin.
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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.