Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/198210
Type: Artigo de periódico
Title: Arhgap21 Modulates Fak Activity And Impairs Glioblastoma Cell Migration.
Author: Bigarella, Carolina Louzão
Borges, Luciene
Costa, Fernando Ferreira
Saad, Sara Terezinha Olalla
Abstract: Glioblastoma multiforme is highly aggressive and is the most common glial tumor type. Although there have been advances in treatment, the average survival expectancy is 12-15 months. Several genes have been shown to influence glioblastoma progression. In the present work, we demonstrate that the RhoGTPase Activating Protein 21 (ARHGAP21) is expressed in the nuclear and perinuclear regions of several cell lines. In T98G and U138MG, glioblastoma derived cell lines, ARHGAP21 interacts with the C-terminal region of Focal Adhesion Kinase (FAK). ARHGAP21 depletion by shRNAi in T98G cells alters cellular morphology and increases: FAK phosphorylation states and activation of downstream signaling; the activity state of Cdc42; the production of metalloproteinase 2 (MMP-2) and cell migration rates. These modifications were found to be mainly due to the loss of ARHGAP21 action on FAK and, consequently, the activation of downstream effectors. These results suggest not only that ARHGAP21 might act as a tumor suppressor gene, but also indicate that ARHGAP21 might be a master regulator of migration having a crucial role in controlling the progression of different tumor types.
Subject: Actins
Animals
Cell Line, Tumor
Cell Movement
Cell Shape
Crk-associated Substrate Protein
Cytoskeleton
Focal Adhesion Kinase 1
Gtpase-activating Proteins
Glioblastoma
Humans
Matrix Metalloproteinase 2
Rna Interference
Signal Transduction
Cdc42 Gtp-binding Protein
Src-family Kinases
Rights: fechado
Identifier DOI: 10.1016/j.bbamcr.2009.02.010
Address: http://www.ncbi.nlm.nih.gov/pubmed/19268501
Date Issue: 2009
Appears in Collections:Unicamp - Artigos e Outros Documentos

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