Boric Acid Induces Oxidative Damage and Apoptosis Through <scp>SEMA3A</scp> / <scp>PLXNA1</scp> / <scp>NRP1</scp> Signalling Pathway in <scp>U251</scp> Glioblastoma Cell

Glioblastoma is one of the deadliest cancers with a very low chance of survival. Glioblastomas have a poor prognosis because of their infiltrative nature, which makes them difficult to totally isolate with rigorous surgery, radiation, and chemotherapy. Our aim in this study was to investigate the efficacy of boric acid, which has anti-cancer properties, on glioblastoma, which has very limited treatment options. U251 human glioblastoma cell lines were treated with IC25 (15.62 μg/mL), IC50 (31.25 μg/mL) and IC75 (62.5 μg/mL) doses of boric acid. Cell viability and proliferation levels were tested. At the same time, the activity of boric acid on cells was tested through oxidative stress, apoptosis, and semaphorin signalling pathway parameters. Our findings indicate that boric acid induced dose-dependent oxidative stress, cellular growth inhibition, apoptosis and morphological changes in U251 cells. Additionally, treatments with increasing amounts of boric acid resulted in a rise in the production of biomarkers of the semaphorin pathway, which may limit cell growth and proliferation. We found that boric acid activates apoptosis by triggering ROS formation at high doses and at the same time inhibits cell proliferation by increasing semaphorin signalling pathway expressions. Boric acid may act as an anti-cancer agent by activating different mechanisms in a dose-dependent manner.