ArticleBrain pathology (Zurich, Switzerland)2009
Altered adhesive structures and their relation to RhoGTPase activation in merlin-deficient Schwannoma.
Article in Brain pathology (Zurich, Switzerland), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
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- Proteomic screening identifies PML/p53 axis as a potential treatment target of facial nerve schwannomas.American journal of translational research · 2020Article
- YAP/TAZ Inhibition Induces Metabolic and Signaling Rewiring Resulting in Targetable Vulnerabilities in NF2-Deficient Tumor Cells.Developmental cell · 2019Article
- Cellular prion protein (PrPOncogene · 2017Article
- p53 performs an essential role in mediating the oncogenic stimulus triggered by loss of expression of neurofibromatosis type 2 duringOncology letters · 2017Article
- Tissue-engineered rhesus monkey nerve grafts for the repair of long ulnar nerve defects: similar outcomes to autologous nerve grafts.Neural regeneration research · 2016Article
- Role of Merlin/NF2 inactivation in tumor biology.Oncogene · 2016Review
- Loss of SOX10 function contributes to the phenotype of human Merlin-null schwannoma cells.Brain : a journal of neurology · 2013Article
- Rac1 controls Schwann cell myelination through cAMP and NF2/merlin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms.Acta neuropathologica · 2012Review
- What's new in neurofibromatosis? Proceedings from the 2009 NF Conference: new frontiers.American journal of medical genetics. Part A · 2010Article
- PAK kinase regulates Rac GTPase and is a potential target in human schwannomas.Experimental neurology · 2009Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schwannomas are Schwann cell tumors of the nervous system that occur spontaneously and in patients with neurofibromatosis 2 (NF2) and lack the tumor suppressor merlin. Merlin is known to bind paxillin, beta1 integrin and focal adhesion kinase, members of focal contacts, multi-protein complexes that mediate cell adhesion to the extracellular matrix. Moreover, merlin-deficient Schwannomas show pathological adhesion to the extracellular matrix making the characterization of focal contacts indispensable. Using our Schwannoma in vitro model of human primary Schwann and Schwannoma cells, we here show that Schwannoma cells display an increased number of mature and stable focal contacts. In addition to an involvement of RhoA signaling via the Rho kinase ROCK, Rac1 plays a significant role in the pathological adhesion of Schwannoma cells. The Rac1 guanine exchange factor- beta-Pix, localizes to focal contacts in human primary Schwannoma cells, and we show that part of the Rac1 activation, an effect of merlin-deficiency, occurs at the level of focal contacts in human primary Schwannoma cells. Our results help explaining the pathological adhesion of Schwannoma cells, further strengthen the importance of RhoGTPase signaling in Schwannoma development, and suggest that merlin's role in tumor suppression is linked to focal contacts.
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