Boric Acid Affects Cell Proliferation, Apoptosis, and Oxidative Stress in ALL Cells
Büşra Hilal1, Aslı Eldem2, Tuba Oz2
1Faculty of Medicine, Izmir Katip Celebi University, Izmir, Turkey.
Biological Trace Element Research
|November 28, 2023
Summary
Boric acid (BA) shows potential as an anti-cancer agent for T-cell acute lymphoblastic leukemia (T-ALL). It inhibits cancer cell proliferation and induces apoptosis, offering a less toxic therapeutic option.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- T-cell acute lymphoblastic leukemia (T-ALL) presents challenges due to chemo-resistance and the need for less toxic therapies.
- Elemental boron, particularly boric acid (BA), exhibits cytotoxic properties against cancer cells, warranting further investigation.
Purpose of the Study:
- To investigate the effects of boric acid (BA) on cell proliferation, apoptosis, and oxidative stress in Jurkat cells, a model for T-ALL.
- To evaluate BA's potential as an anti-cancer therapeutic agent for T-ALL.
Main Methods:
- Cell viability assessed using XTT assay to determine IC50 concentration.
- Apoptosis analyzed via acridine orange/ethidium bromide staining and gene expression of apoptosis regulators (Bcl-2, Bax, Caspase-3-8-9) and miR-21 using RT-qPCR.
- Oxidative stress markers (TOS, TAS, OSI) were quantified.
Main Results:
- Boric acid demonstrated dose-dependent inhibition of Jurkat cell proliferation with an IC50 of 802.7 μg/mL.
- BA induced apoptosis by downregulating anti-apoptotic genes and upregulating pro-apoptotic genes, alongside a significant reduction in miR-21 expression.
- BA treatment increased total antioxidant status (TAS) and decreased total oxidant status (TOS) in Jurkat cells.
Conclusions:
- Boric acid exhibits cytotoxic effects on Jurkat cells, inhibiting proliferation and inducing apoptosis.
- BA modulates the expression of key apoptosis-related genes and microRNA, suggesting a role in programmed cell death.
- The findings support boric acid as a potential anti-cancer agent for T-ALL, acting through antiproliferative and pro-apoptotic mechanisms with effects on cellular redox balance.
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