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Original Paper

Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Bauer R.2,6,* · Ratzinger S.3,6,* · Wales L.1,6 · Bosserhoff A.4 · Senner V.5 · Grifka J.1 · Grässel S.1,6

Corresponding Author

Susanne Grässel, Ph.D.

Department of Orthopaedic Surgery, University Hospital Regensburg

ZMB / BioPark 1, Josef-Engert-Str. 9, 93053 Regensburg (Germany)

Tel. +49-941-943-5065, Fax +49-941-943-5066

E-Mail susanne.graessel@klinik.uni-regensburg.de

Related Articles for ""

Cell Physiol Biochem 2011;27:217–226

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Glioblastomas are characterized by an intense local invasiveness that limits surgical resection. One mechanism by which glioma cells enforce their migration into brain tissue is reorganization of tumour associated extracellular matrix (ECM). Collagen XVI is a minor component of connective tissues. However, in glioblastoma tissue it is dramatically upregulated compared to the ECM of normal cortex. The aim of this study is to delineate tumour cell invasion and underlying mechanisms involving collagen XVI by using a siRNA mediated collagen XVI knockdown model in U87MG human glioblastoma cells. Knockdown of collagen XVI resulted in decreased invasiveness in Boyden chamber assays, and in a reduction of focal adhesion contact numbers per cell. Gene expression was upregulated for protocadherin 18 and downregulated for kindlin-1 and -2. Proliferation was not affected while flow cytometric analysis demonstrated reduced β1-integrin activation in collagen XVI knockdown cells. We suggest that in glioblastoma tissue collagen XVI may impair the cell-cell interaction in favour of enhancement of invasion. The modification of the β1-integrin activation pattern through collagen XVI might be a molecular mechanism to further augment the invasive phenotype of glioma cells. Elucidating the underlying mechanisms of glioma cell invasion promoted by collagen XVI may provide novel cancer therapeutic approaches in neurooncology.

© 2011 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: March 01, 2011
Published online: April 01, 2011
Issue release date: April 2011

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

For additional information: https://www.karger.com/CPB

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