2ⁿᵈ Edition of the Cancer R&D World Conference 2026

Abstract

Background: Glioblastomas (U87) are an aggressive brain tumor that arises from glial cells and invades surrounding parts of the brain. The prognosis for glioblastoma is poor, with a median survival rate of 15 months with treatment. Treatments are aggressive with severe side effects. Molecular therapeutics are required to control U87 cell growth with a better safety profile. Several plant-derived compounds were tested for chemo preventive effects against glioblastoma. However, the role of Epimedin A, isolated from the genus of low-growing plants known as Epimedium (Horny Goat Weed), in preventing cancer growth is not clear.

Purpose: We examined the chemo preventive effects of Epimedin A in U87 cells. We specifically investigated the effects it has on cell proliferation, apoptosis, oxidative signaling, and migration.

Methods: U87 cells obtained from ATCC were treated with an increasing concentration of Epimedin A (0-100 uM) ± EGF. Cell viability was examined using the MTT assay, while invasion and migration were assessed by scratch and transwell migration assays, respectively. Expression of various apoptotic proteins was measured by an antibody array. Reactive oxygen species levels were measured using fluorescence-based assay. Statistical comparisons were performed using one sided t test for a prespecified directional hypothesis and reported using mean ± standard deviation.

Results: Our results suggest that Epimedin A prevents the growth of U87 cells in a dose-dependent manner, with 60µM producing the greatest reduction in cell proliferation under EGF stimulation.

Furthermore, Epimedin-A also prevented the invasion and migration of U87 cancer cells. Additionally, Epimedin A increased caspase-3 expression, as measured by PARP cleavage under EGF stimulation, and reduced the formation of reactive oxygen species. Epimedin A also regulates the expression of various pro- and anti-apoptotic proteins such as Bcl-x, HIF-1alpha, Bad, Bax, cleaved Caspase-3, Cytochrome C, SMAC/Diablo.

Conclusion: Epimedin A has displayed inhibitory effects on U87 cells' viability. Specifically, studies showed inhibitory effects on proliferation, migration, and ROS. Further, Epimedin A regulates the expression of various pro- and anti-apoptotic factors and inflammatory markers in cancer cells. We next planned to examine its in vivo efficacy using nude mice xenografts. Thus, our results indicate that Epimedin A inhibits the growth of U87 cells and may act as a chemo preventive agent.