Inhibition of human glioblastoma multiforme cells by 10,11-dehydrocur- vularin through the MMP-2 and PI3K/AKT signaling pathways

Glioblastoma, formerly known as glioblastoma multiforme (GBM), is a malignant nervous system tumor with high morbidity, recurrence rate, and mortality. Treating glioblastoma is difficult due to complicating factors, and novel therapeutic strategies are required to overcome resistance. In this study, we investigate the glioblastoma inhibitory activity of 10,11-dehydrocurvularin (DCV), a polyketide compound with broad biological activities, despite the fact that its anti-glioma properties and related mechanisms have yet to be studied. We look at how DCV affects glioblastoma cell lines U251 and U87 versus HEB cells. We discover that DCV inhibits glioblastoma cell proliferation, colony formation, migration, and invasion, as well as causing cell apoptosis. DCV treatment inhibits AKT phosphorylation and decreases the level of the PI3K/AKT pathway downstream protein MMP2. Our findings suggest that DCV could be a candidate for developing more potent glioblastoma chemotherapeutic drugs.

Automated summary

Glioblastoma is a highly deadly malignant nervous system tumor that is difficult to treat. This study investigated the inhibitory effects of the compound DCV on glioblastoma and discovered its potential as a candidate for developing more potent chemotherapy drugs.