Effect of Electrical Capacitance-Based Therapy on the Viability of U87 and T98-G Glioblastoma Cell Lines
Turkish Neurosurgery, cilt.36, sa.5, ss.658-663, 2026 (SCI-Expanded, Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 36 Sayı: 5
- Basım Tarihi: 2026
- Doi Numarası: 10.5137/1019-5149.jtn.49048-25.3
- Dergi Adı: Turkish Neurosurgery
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, MEDLINE, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.658-663
- Anahtar Kelimeler: Apoptosis, Cell viability, Electric field therapy, Electro-capacitive cancer therapy, Glioblastoma
- Kayseri Üniversitesi Adresli: Evet
Özet
AIM: To examine the selective cytotoxic effects of Electro-Capacitive Cancer Therapy (ECCT) on human glioblastoma (GBM) cell lines (U87-MG and T98-G) and to evaluate its impact on normal epithelial cells. MATERIAL and METHODS: U87-MG and T98-G glioblastoma cells, along with Beas-2B normal epithelial cells, were exposed to ECCT at 100 kHz frequency and 20 V for 24 hours. Cell viability was determined using the MTT assay, while morphological changes were assessed through phase-contrast microscopy. Statistical analyses were conducted using one-way ANOVA and Student's t-test, with statistical significance defined as p < 0.05. RESULTS: ECCT exposure caused a time-dependent reduction in the viability of both GBM cell lines. U87-MG cells showed significant inhibition at all exposure durations, whereas T98-G cells exhibited a marked decrease only after 24 hours (p < 0.0001). In contrast, Beas-2B cells maintained their morphology and viability, suggesting that ECCT selectively targets malignant cells while sparing normal epithelial cells. CONCLUSION: ECCT significantly inhibits glioblastoma cell proliferation without adversely affecting normal cells, highlighting its promise as a non-invasive adjunctive treatment option for GBM. Further preclinical and clinical studies are warranted to clarify its underlying mechanisms, optimize exposure parameters, and determine its potential integration into multimodal glioblastoma therapy.