Expression of Activin A and Follistatin in Glioblastoma and Their Effects on U87 In Vitro

Abstract

In some cancer cell lines, the gene encoding activin A ( inhibin β A [ INHBA]) is over-expressed and enhances cancer proliferation. Protein levels of activin A and follistatin were assessed in glioblastoma and normal brain tissues in this study, and the effect of activin A and follistatin treatment on the proliferation of U87 human glioblastoma cells in vitro was also studied. High levels of activin A were observed in glioblastomas compared with normal brain tissue. In contrast, follistatin levels were similar between the two tissues. [3H]Thymidine assay showed that activin A (3–30 ng/ml) produced a dose-dependent increase in DNA synthesis of U87 cells compared with controls. Flow cytometric analyses showed that activin A increased the proliferative index of U87 cells compared with controls. Activin A also induced up-regulation of p-SMAD2/3 in a dose-dependent manner. Treatment of U87 cells with follistatin blocked these activin A-induced effects. The disequilibrium between activin A and follistatin may play a role in the development of glioblastoma.