Induction of proline-rich tyrosine kinase 2 activation-mediated C6 glioma cell invasion after anti-vascular endothelial growth factor therapy.

ABSTRACT:

Background

Anti-angiogenic therapy inhibits tumor growth and is considered as a potential clinical therapy for malignant glioma. However, inevitable recurrences and unexpected tumor resistance, particularly increased invasion ability of glioma cell, were observed after anti-angiogenic treatment. The underlying mechanism remains undetermined. Focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) are closely associated with cell migration; therefore, we investigated the possible role of these kinases in rat C6 glioma cell invasion induced by bevacizumab, a recombinant monoclonal antibody against vascular endothelial growth factor (VEGF).

Methods

The effects of bevacizumab on migration and invasion of C6 glioma cells were investigated in vitro and in vivo. The c

SUBMITTER: Xu CS 

PROVIDER: S-EPMC4049398 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature