ArticleOncogene2010
Plakoglobin interacts with and increases the protein levels of metastasis suppressor Nm23-H2 and regulates the expression of Nm23-H1.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Mechanisms of non-metastatic 2 (NME2)-mediated control of metastasis across tumor types.Naunyn-Schmiedeberg's archives of pharmacology · 2011Pooled it
- Transcriptional deregulation by FOXM1-JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance.Cell communication and signaling : CCS · 2025Article
- Junction Plakoglobin - A Dual-Role Player in Cancer Biology.International journal of surgery (London, England) · 2025Review
- Plakoglobin does not participate in endothelial barrier stabilization mediated by cAMP.Scientific reports · 2025Article
- Paradoxical Roles of Desmosomal Components in Head and Neck Cancer.Biomolecules · 2021Review
- Loss of the Metastasis Suppressor NME1, But Not of Its Highly Related Isoform NME2, Induces a Hybrid Epithelial-Mesenchymal State in Cancer Cells.International journal of molecular sciences · 2021Article
- Junction plakoglobin regulates and destabilizes HIF2α to inhibit tumorigenesis of renal cell carcinoma.Cancer communications (London, England) · 2021Article
- Activation of Nm23-H1 to suppress breast cancer metastasis via redox regulation.Experimental & molecular medicine · 2021Review
- Increased expression of plakoglobin is associated with upregulated MAPK and PI3K/AKT signalling pathways in early resectable pancreatic ductal adenocarcinoma.Oncology letters · 2020Article
- Quassinoid analogs with enhanced efficacy for treatment of hematologic malignancies target the PI3Kγ isoform.Communications biology · 2020Article
- Small molecule activator of Nm23/NDPK as an inhibitor of metastasis.Scientific reports · 2018Article
- Plakoglobin restores tumor suppressor activity of p53Cancer science · 2018Article
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Disrupted IRF6-NME1/2 Complexes as a Cause of Cleft Lip/Palate.Journal of dental research · 2017Article
- Beyond cell-cell adhesion: Plakoglobin and the regulation of tumorigenesis and metastasis.Oncotarget · 2017Review
- The physical interaction of p53 and plakoglobin is necessary for their synergistic inhibition of migration and invasion.Oncotarget · 2016Article
- Plakoglobin Reduces the in vitro Growth, Migration and Invasion of Ovarian Cancer Cells Expressing N-Cadherin and Mutant p53.PloS one · 2016Article
- Desmosome regulation and signaling in disease.Cell and tissue research · 2015Review
- Regulatory functions of Nm23-H2 in tumorigenesis: insights from biochemical to clinical perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- Modulation of cytoskeletal dynamics by mammalian nucleoside diphosphate kinase (NDPK) proteins.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Plakoglobin (gamma-catenin) is a homolog of beta-catenin with similar dual adhesive and signaling functions. The adhesive function of these proteins is mediated by their interactions with cadherins, whereas their signaling activity is regulated by association with various intracellular partners. In this respect, beta-catenin has a well-defined oncogenic activity through its role in the Wnt signaling pathway, whereas plakoglobin acts as a tumor/metastasis suppressor through mechanisms that remain unclear. We previously expressed plakoglobin in SCC9 squamous carcinoma cells (SCC9-P) and observed a mesenchymal-to-epidermoid transition. Comparison of the protein and RNA profiles of parental SCC9 cells and SCC9-P transfectants identified various differentially expressed proteins and transcripts, including the nonmetastatic protein 23 (Nm23). In this study, we show that Nm23-H1 mRNA and Nm23-H2 protein are increased after plakoglobin expression. Coimmunoprecipitation and confocal microscopy studies using SCC9-P and various epithelial cell lines with endogenous plakoglobin expression revealed that Nm23 interacts with plakoglobin, cadherins and alpha-catenin. Furthermore, Nm23-H2 is the primary isoform involved in these interactions, which occur prominently in the cytoskeleton-associated pool of cellular proteins. In addition, we show that plakoglobin-Nm23 interaction requires the N-terminal (alpha-catenin interacting) domain of plakoglobin. Our data suggest that by increasing the expression and stability of Nm23, plakoglobin has a role in regulating the metastasis suppressor activity of Nm23, which may further provide a potential mechanism for the tumor/metastasis suppressor function of plakoglobin itself.
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Registered trials
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