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Boric Acid Affects the Expression of DNA Double-Strand Break Repair Factors in A549 Cells and A549 Cancer Stem Cells:

Tuğba Semerci Sevimli1, Aynaz Ghorbani2, Bahar Demir Cevizlidere2

  • 1Cellular Therapy and Stem Cell Production, Application, and Research Center (ESTEM), Eskişehir Osmangazi University, Eskişehir, 26040, Turkey. tssevimli@ogu.edu.tr.

Biological Trace Element Research
|February 17, 2024
PubMed

Insights

Boric acid (BA) impacts DNA double-strand break (DSB) repair and apoptosis in lung cancer stem cells (LC-SCs). BA significantly increased ATM expression and upregulated caspase-3 and E-cadherin, suggesting a role in cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • DNA double-strand break (DSB) repair genes are crucial in cancer stem cell (CSC) processes like stemness and resistance.
  • Targeting DSB repair pathways is a key strategy for cancer treatment, particularly for the CSC phenotype.
  • The specific effects of boric acid (BA) on DSB repair in lung cancer stem cells (LC-SCs) remain largely unexplored.

Purpose of the Study:

  • To investigate the effects of boric acid (BA) on DNA double-strand break (DSB) repair mechanisms and apoptotic pathways in A549 lung cancer stem cells (LC-SCs).

Main Methods:

  • Cancer stem cells (CSCs) were isolated from A549 human non-small cell lung cancer cells and characterized.
  • Cells were treated with varying concentrations of boric acid (1-100 mM).
  • Cell viability was assessed using MTT assays; gene expression of DSB repair genes (BRCA1, BRCA2, RAD51, KU70/80, ATM, XRCC4) was analyzed via RT-qPCR; and caspase-3 and E-cadherin expression were evaluated by immunofluorescence.

Main Results:

  • Boric acid treatment led to a significant increase in ATM gene expression (p < 0.001) in LC-SCs.
  • No significant changes were observed in the expression of other investigated DSB repair genes (BRCA1, BRCA2, RAD51, KU70/80, XRCC4).
  • Boric acid upregulated the expression of caspase-3 and E-cadherin, indicating an impact on apoptosis and potentially cell adhesion.

Conclusions:

  • Boric acid influences DNA double-strand break (DSB) repair pathways in lung cancer stem cells (LC-SCs), specifically by upregulating ATM expression.
  • BA enhances the apoptotic potential of LC-SCs, as evidenced by increased caspase-3 expression.
  • These findings suggest that boric acid may represent a therapeutic agent targeting CSCs by modulating DSB repair and apoptosis.
Keywords:
Boric acidCytotoxicityDNA DSBLung cancer stem cell

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