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Knockdown of annexin 2 decreases migration of human glioma cells in vitro.
Tatenhorst, L; Rescher, U; Gerke, V; Paulus, W.
Afiliação
  • Tatenhorst L; Institute of Neuropathology, University Hospital Muenster, Muenster, Germany.
Neuropathol Appl Neurobiol ; 32(3): 271-7, 2006 Jun.
Article em En | MEDLINE | ID: mdl-16640645
Diffuse invasion of brain tissue is a major reason for the poor prognosis of patients with glioblastoma. Annexin 2, a member of the large annexin family of Ca2+ and membrane-binding proteins, is expressed at high protein levels in human gliomas and has been proposed as a marker of glioma malignancy, while its functional role in these tumours is unknown so far. The ability of annexin 2 to interact with the actin cytoskeleton, as well as its potential to bind invasion-associated proteases, suggests that it could participate in invasion-associated processes in human gliomas. Therefore, we analysed here functional consequences of RNA interference-mediated silencing of annexin 2 in U87MG and U373MG human glioma cell lines. While no impact of annexin 2 downregulation on proliferation and adhesion was observed, our analyses revealed that migration of U87MG and U373MG cells was significantly inhibited following annexin 2 depletion. This effect was not related to a compensatory increase of the related annexins 1 or 6. Our findings identify annexin 2 as a potential candidate involved in glioma invasion and support the potential of RNA interference as powerful tool in the decryption of glioma invasion mechanisms.
Assuntos
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Base de dados: MEDLINE Assunto principal: Neoplasias Encefálicas / Movimento Celular / Anexina A2 / Glioma / Invasividade Neoplásica Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Neuropathol Appl Neurobiol Ano de publicação: 2006 Tipo de documento: Article País de afiliação: Alemanha
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Base de dados: MEDLINE Assunto principal: Neoplasias Encefálicas / Movimento Celular / Anexina A2 / Glioma / Invasividade Neoplásica Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Neuropathol Appl Neurobiol Ano de publicação: 2006 Tipo de documento: Article País de afiliação: Alemanha