ArticleStem cells and development2014
Netrin-1 induces MMP-12-dependent E-cadherin degradation via the distinct activation of PKCα and FAK/Fyn in promoting mesenchymal stem cell motility.
Article in Stem cells and development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Electronic cigarette aerosols disrupt airway barrier function via MMP-dependent E-cadherin cleavage: findings from cell culture and murine models.Archives of toxicology · 2026Article
- S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models.The Journal of clinical investigation · 2025Article
- The Role of Macrophage-Derived Netrin-1 in Inflammatory Diseases.Biomolecules · 2025Review
- Netrin-1 Is an Important Mediator in Microglia Migration.International journal of molecular sciences · 2024Article
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- Netrin-1 induces the anti-apoptotic and pro-survival effects of B-ALL cells through the Unc5b-MAPK axis.Cell communication and signaling : CCS · 2022Article
- Nanotechnology and Matrix Metalloproteinases in Cancer Diagnosis and Treatment.Frontiers in molecular biosciences · 2022Review
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- UNC5C‑knockdown enhances the growth and metastasis of breast cancer cells by potentiating the integrin α6/β4 signaling pathway.International journal of oncology · 2020Article
- Dependence and Guidance Receptors-DCC and Neogenin-In Partial EMT and the Actions of Serine Proteases.Frontiers in oncology · 2020Review
- Efficient Neural Differentiation of hPSCs by Extrinsic Signals Derived from Co-cultured Neural Stem or Precursor Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
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- MiR-1284 suppresses gastric cancer progression by targeting EIF4A1.OncoTargets and therapy · 2019Article
- Serine protease modulation of Dependence Receptors and EMT protein expression.Cancer biology & therapy · 2019Article
- Making Connections: Guidance Cues and Receptors at Nonneural Cell-Cell Junctions.Cold Spring Harbor perspectives in biology · 2018Review
- Matrix metalloproteinase-12 as an endogenous resolution promoting factor following myocardial infarction.Pharmacological research · 2018Review
- Effect of Different Preconditioning Regimens on the Expression Profile of Murine Adipose-Derived Stromal/Stem Cells.International journal of molecular sciences · 2018Article
- Regulation of cell proliferation and metastasis by microRNA-593-5p in human gastric cancer.OncoTargets and therapy · 2018Article
- Article
- Netrin-1 promotes gastric cancer cell proliferation and invasion via the receptor neogenin through PI3K/AKT signaling pathway.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Netrin-1 (Ntn-1) is a potent inducer of neuronal cell migration; however, its molecular mechanism that guides the migratory behavior of stem cells has not been characterized. In this study, we investigate the role of Ntn-1 in promoting the motility of human umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs) and its related signaling pathways. Ntn-1 (50 ng/mL) significantly increased motility of UCB-MSCs, which was inhibited by blocking antibodies for deleted in colorectal cancer (DCC) and integrin (IN) α6β4. Ntn-1 in DCC stimulated protein kinase Cα (PKCα) activation, but not PKCɛ, PKCθ, and PKCζ, while Ntn-1 in INα6β4 induced the phosphorylation of focal adhesion kinase (FAK) and Fyn. Notably, Ntn-1 induced phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and nuclear factor kappa-B (NF-κB), but they were concurrently downregulated by blocking the activities of PKCα, FAK, and Fyn. Ntn-1 uniquely increased the MMP-12 expression of all the matrix metalloproteinase (MMP) isoforms present in UCB-MSCs, though this was significantly blocked by an NF-κB inhibitor. Finally, Ntn-1 induced the MMP-12-dependent degradation of E-cadherin (E-cad), while Ntn-1 abrogated the interaction between E-cad and p120-catenin. In addition, Ntn-1 has the ability to stimulate cytoskeletal reorganization-related proteins, such as Cdc42, Rac1, Profilin-1, Cofilin-1, α-Actinin-4, and filamentous actin (F-actin) in UCB-MSCs. These results demonstrate that Ntn-1 induces MMP-12-dependent E-cad degradation via the distinct activation of PKCα and FAK/Fyn, which is necessary to govern the activation of ERK, JNK, and NF-κB in promoting motility of UCB-MSCs.
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Registered trials
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