Prazosin inhibits the proliferation, migration and invasion, but promotes the apoptosis of U251 and U87 cells via the PI3K/AKT/mTOR signaling pathway.

Prazosin, an α-adrenergic receptor antagonist, is used to treat mild to moderate hypertension. It has recently been discovered that α-adrenergic receptors may have potential antitumor properties. Therefore, in the present study, the effect of prazosin on human glioblastoma and the underlying mechanism were investigated. Human glioblastoma U251 and U87 cells were treated with different concentrations of prazosin, and a Cell Counting Kit-8 assay was performed to investigate the effects of prazosin on cell proliferation. Transwell migration and invasion assays were used to assess the effects of prazosin on cell migration and invasion. Prazosin-induced apoptosis in U251 and U87 cells was detected by flow cytometry, and the protein expression levels of anti-apoptotic proteins and proteins related to the PI3K/AKT/mTOR signaling pathway were detected by western blotting. The results suggested that following treatment with prazosin, the proliferation, migration and invasion of U251 and U81 cells were decreased. By contrast, U251 and U81 cell apoptosis, as well as the protein expression levels of Bax and active Caspase-3 were increased after prazosin treatment (P<0.05). Bcl-2 levels were also decreased after prazosin treatment (P<0.05). Additionally, the expression of phosphorylated (p)-AKT and p-mTOR, P70 and cyclin D1 were decreased in U251 and U81 cells following prazosin treatment (P<0.05). The present study suggested that prazosin may suppress glioblastoma progression by downregulating the activity of the PI3K/AKT/mTOR signaling pathway.