NDLI: uPAR and cathepsin B shRNA impedes TGF-ß1-driven proliferation and invasion of meningioma cells in a XIAP-dependent pathway.

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uPAR and cathepsin B shRNA impedes TGF-ß1-driven proliferation and invasion of meningioma cells in a XIAP-dependent pathway.

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uPAR and cathepsin B shRNA impedes TGF-ß1-driven proliferation and invasion of meningioma cells in a XIAP-dependent pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gogineni, V. R. Gupta, R. Nalla, A. K. Velpula, K. K. Rao, J. S.
Description	Country affiliation: United States Author Affiliation: Gogineni VR ( Department of Cancer Biology & Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL 61605, USA.)
Abstract	Overexpression of transforming growth factor ß1 (TGF-ß1) has been linked to immune suppression, tumor angiogenesis, tumor cell migration, tumor cell survival, and tumor cell invasion in many cancers. In the present study, we found abundant expression of TGF-ß1 in the microenvironment of four different pathological types of meningioma tumors. TGF-ß1 induced invasion in malignant meningioma cells with an associated upregulation of urokinase-type plasminogen activator (uPA), uPAR, cathepsin B, and MMP-9, and this increase in proliferation was coupled with the expression of anti-apoptotic and pro-survival signaling molecules. In addition to the intense immunoreactivity of meningioma tumors to X-linked inhibitor to apoptosis (XIAP), its knockdown abolished the TGF-ß1-induced proliferation of these cells. The stimulation of XIAP expression and the activation of pSMAD-2 is mediated by phosphatidylinositol 3-kinase (PI3K)- and MEK-dependent pathways, and the addition of anti-TGF-ß1 antibodies prevented their expression with a consequent decrease in invasion. Bicistronic shRNA constructs targeting uPAR and cathepsin B (pUC) quenched TGF-ß1-driven invasion and survival of meningioma cells by downregulation of XIAP and pSMAD-2 expression. Animal models with intracranial tumors showed elevated levels of TGF-ß1, XIAP and pSMAD-2, and pUC treatment prevented this increased expression. Thus, targeted silencing of TGF-ß1-induced signaling by pUC in meningioma would provide new treatment approaches for management of meningioma.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.170
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-12-06
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Meningeal Neoplasms Research Support, N.i.h., Extramural Cell Proliferation Rna, Small Interfering Transforming Growth Factor Beta1 Neoplasm Invasiveness Gene Expression Regulation, Neoplastic Metabolism Rna Interference Physiopathology Receptors, Urokinase Plasminogen Activator Discipline Cell Biology Pathology Down-regulation Cathepsin B Cell Line, Tumor Genetics X-linked Inhibitor Of Apoptosis Protein Meningioma
Content Type	Text
Resource Type	Article

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