ArticlePloS one2013
The expression of the Nectin complex in human breast cancer and the role of Nectin-3 in the control of tight junctions during metastasis.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Disruption of thrombospondin 1/2-integrin β1 axis impairs cell adhesion and tumor growth in intrahepatic cholangiocarcinoma.Cell death discovery · 2026Article
- Spatial multi-omics characterization of neuroblastoma reveals ferroptosis-associated metabolic features in high-risk tumors.Genome medicine · 2026Article
- Functional and in silico evidence for the role of microRNAs 148a-5p and 199a in migration and invasion of papillary thyroid carcinoma cells.Discover oncology · 2025Article
- The Significance of Nectin Family Proteins in Various Cancerogenous Processes.International journal of molecular sciences · 2025Review
- Review
- Pathophysiology in Brain Arteriovenous Malformations: Focus on Endothelial Dysfunctions and Endothelial-to-Mesenchymal Transition.Biomedicines · 2024Review
- Metastasis suppressor genes in clinical practice: are they druggable?Cancer metastasis reviews · 2023Review
- Expression of Claudin-9 (CLDN9) in Breast Cancer, the Clinical Significance in Connection with Its Subcoat Anchorage Proteins ZO-1 and ZO-3 and Impact on Drug Resistance.Biomedicines · 2023Article
- Prognostic Potential of Nectin Expressions in Colorectal Cancer: An Exploratory Study.International journal of molecular sciences · 2023Article
- Review
- Nectins and Nectin-like Molecules in Colorectal Cancer: Role in Diagnostics, Prognostic Values, and Emerging Treatment Options: A Literature Review.Diagnostics (Basel, Switzerland) · 2022Review
- Claudin5 protects the peripheral endothelial barrier in an organ and vessel-type-specific manner.eLife · 2022Article
- Multiphoton Microscopy Reveals DAPK1-Dependent Extracellular Matrix Remodeling in a Chorioallantoic Membrane (CAM) Model.Cancers · 2022Article
- Article
- Mechanisms Ensuring Endothelial Junction Integrity Beyond VE-Cadherin.Frontiers in physiology · 2020Review
- Dysregulation of adenosine kinase isoforms in breast cancer.Oncotarget · 2019Article
- Nectin-2 in ovarian cancer: How is it expressed and what might be its functional role?Cancer science · 2019Article
- Article
- Virus-Receptor Interactions: Structural Insights For Oncolytic Virus Development.Oncolytic virotherapy · 2019Review
- Enhanced Sensitivity of Patient-Derived Pediatric High-Grade Brain Tumor Xenografts to Oncolytic HSV-1 Virotherapy Correlates with Nectin-1 Expression.Scientific reports · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNectins are a family of integral protein molecules involved in the formation of functioning Adherens and Tight Junctions (TJ). Aberrant expression is associated with cancer progression but little is known how this effects changes in cell behaviour. This study aimed to ascertain the distribution of Nectins-1 to -4 in human breast cancer and the effect on junctional integrity of Nectin-3 modulation in human endothelial and breast cancer cells.
methodsA human breast tissue cohort was processed for Q-PCR and immunohistochemistry for analysis of Nectin-1/-2/-3/-4. Nectin-3 over-expression was induced in the human breast cancer cell line MDA-MB-231 and the human endothelial cell line HECV. Functional testing was carried out to ascertain changes in cell behaviour.
resultsQ-PCR revealed a distinct reduction in node positive tumours and in patients with poor outcome. There was increased expression of Nectin-1/-2 in patients with metastatic disease, Nectin-3/-4 was reduced. IHC revealed that Nectin-3 expression showed clear changes in distribution between normal and cancerous cells. Nectin-3 over-expression in MDA-MB-231 cells showed reduced invasion and migration even when treated with HGF. Changes in barrier function resulted in MDAN3 cells showing less change in resistance after 2h treatment with HGF (p<0.001). Nectin-3 transformed endothelial cells were significantly more adhesive, irrespective of treatment with HGF (p<0.05) and had reduced growth. Barrier function revealed that transformed HECV cells had significantly tighter junctions that wildtype cells when treated with HGF (p<0.0001). HGF-induced changes in permeability were also reduced. Overexpression of Nectin-3 produced endothelial cells with significantly reduced ability to form tubules (p<0.0001). Immunoprecipitation studies discovered hitherto novel associations for Nectin-3. Moreover, HGF appeared to exert an effect on Nectin-3 via tyrosine and threonine phosphorylation.
conclusionsNectin-3 may be a key component in the formation of cell junctions and be a putative suppressor molecule to the invasion of breast cancer cells.
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