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<p><i>Purpose</i> Galectin-3 (Gal-3), a multifunctional β-galactoside-binding lectin, is more highly expressed in atypical and anaplastic meningioma subtypes than in normal brain tissue. The mechanism(s) by which Gal-3 may contribute to the aggressive growth of these tumors remains unclear. <i>Methods</i> We evaluated the effects of the Gal-3 inhibitor TD139 combined with either low-intensity direct current electrostimulation (DCES) on meningioma cells in a human co-culture model, or non-invasive transcranial direct current stimulation (tDCS) in an orthotopic preclinical model. <i>Results</i> In vitro, DCES treatment modulated the expression of human leukocyte antigen (HLA) class I and II molecules, which may influence T cell–tumor cell interactions. Gal-3 was found to activate microglia and promote the differentiation of CD4(+) T cells toward Th2 and Treg phenotypes. Treatment with an immunomodulatory dose of DCES, followed by TD139, induced anaplastic meningioma cell death in a human co-culture model without affecting neurons. In the orthotopic allograft preclinical model, treatment with TD139 and tDCS, administered 7 times over 14 days, significantly reduced tumor growth. Survival of tumor-bearing mice treated with TD139 and tDCS was significantly higher than that of untreated controls or mice treated with tDCS or TD139 alone. This combination treatment was also associated with a significant decrease in the meningioma-associated marker NDRG4 and the proliferation marker Ki-67. <i>Conclusion</i> The results indicate that combining Gal-3 inhibitors with direct current stimulation has potential as an effective treatment modality for aggressive meningiomas.</p>

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Effects of Galectin-3 inhibitors paired with direct current stimulation in preclinical models of aggressive meningioma

  • 期刊论文

  • 发表日期：

    2026年6月27日

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  • Arabinda Das,
  • Rachel Malley,
  • Julian E. Bailes,
  • George C. Bobustuc,
  • Abhay K. Varma,
  • Scott M. Lindhorst,
  • David Cachia

摘要

Purpose Galectin-3 (Gal-3), a multifunctional β-galactoside-binding lectin, is more highly expressed in atypical and anaplastic meningioma subtypes than in normal brain tissue. The mechanism(s) by which Gal-3 may contribute to the aggressive growth of these tumors remains unclear. Methods We evaluated the effects of the Gal-3 inhibitor TD139 combined with either low-intensity direct current electrostimulation (DCES) on meningioma cells in a human co-culture model, or non-invasive transcranial direct current stimulation (tDCS) in an orthotopic preclinical model. Results In vitro, DCES treatment modulated the expression of human leukocyte antigen (HLA) class I and II molecules, which may influence T cell–tumor cell interactions. Gal-3 was found to activate microglia and promote the differentiation of CD4(+) T cells toward Th2 and Treg phenotypes. Treatment with an immunomodulatory dose of DCES, followed by TD139, induced anaplastic meningioma cell death in a human co-culture model without affecting neurons. In the orthotopic allograft preclinical model, treatment with TD139 and tDCS, administered 7 times over 14 days, significantly reduced tumor growth. Survival of tumor-bearing mice treated with TD139 and tDCS was significantly higher than that of untreated controls or mice treated with tDCS or TD139 alone. This combination treatment was also associated with a significant decrease in the meningioma-associated marker NDRG4 and the proliferation marker Ki-67. Conclusion The results indicate that combining Gal-3 inhibitors with direct current stimulation has potential as an effective treatment modality for aggressive meningiomas.