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

Ezgi Kar¹, Zeynep Övenler², Ceyhan Hacıoğlu³

¹Department of Nutrition and Dietetics, Faculty of Health Sciences, Kutahya Health Sciences University, Kutahya, Turkey.

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|May 3, 2025

Summary

This summary is machine-generated.

Boric acid shows anti-cancer effects against glioblastoma by inducing oxidative stress and apoptosis while inhibiting cell proliferation via the semaphorin pathway. This study highlights boric acid

Keywords:

apoptosis boric acid glioblastoma oxidative damage semaphorin

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Area of Science:

Oncology
Biochemistry
Cell Biology

Background:

Glioblastoma is a highly aggressive brain tumor with limited treatment options and poor survival rates.
The infiltrative nature of glioblastoma complicates surgical, radiation, and chemotherapeutic interventions.
Boric acid possesses known anti-cancer properties, suggesting potential therapeutic applications.

Purpose of the Study:

To investigate the anti-cancer efficacy of boric acid on human glioblastoma cell lines (U251).
To evaluate the effects of boric acid on cell viability, proliferation, oxidative stress, apoptosis, and the semaphorin signaling pathway.

Main Methods:

U251 human glioblastoma cells were treated with varying doses of boric acid (IC25, IC50, IC75).
Cell viability and proliferation were assessed.
Oxidative stress, apoptosis, and semaphorin pathway biomarkers were analyzed.

Main Results:

Boric acid demonstrated a dose-dependent induction of oxidative stress and apoptosis in U251 cells.
Cellular growth inhibition and morphological changes were observed with boric acid treatment.
Increased semaphorin pathway biomarker production correlated with boric acid dosage, suggesting growth inhibition.

Conclusions:

Boric acid activates apoptosis through reactive oxygen species (ROS) generation at higher doses.
Boric acid inhibits glioblastoma cell proliferation by upregulating the semaphorin signaling pathway.
Boric acid exhibits potential as an anti-cancer agent for glioblastoma through multiple dose-dependent mechanisms.