Boric acid impedes glioblastoma growth in a rat model: insights from multi-approach analysis
Turkez, Hasan, Alper, Fatih, Bayram, Cemil, Baba, Cem, Yildiz, Edanur, Saracoglu, Melik, Kucuk, Muhammed, Gozegir, Berrah, Kiliclioglu, Metin, Yesilyurt, Mustafa, Tozlu, Ozlem Ozdemir, Bolat, Ismail, Yildirim, Serkan, Barutcigil, Muhammed Furkan, Isik, Fatih, Kiki, Ozlem, Aydin, Fahri, Arslan, Mehmet Enes, Cadirci, Kenan, Karaman, Adem, Tatar, Abdulgani, Hacimuftuoglu, Ahmet
Limited advancements in managing malignant brain tumors have resulted in poor prognoses for glioblastoma (GBM) patients. Standard treatment involves surgery, radiotherapy, and chemotherapy, which lack specificity and damage healthy brain tissue. Boron-containing compounds, such as boric acid (BA), exhibit diverse biological effects, including anticancer properties. This study aimed to examine whether boron supplementation, as BA, can inhibit glioblastoma growth in a xenograft animal model. Using MRI-based tumor size measurement, survival rates, hematological, clinical biochemistry analyses, and genotoxicity parameters, we assessed the impact of BA. Histopathological, immunohistochemical, and immunofluorescence examinations were also conducted. All BA doses (3.25, 6.5, and 13 mg kg-1 b.w.) extended survival compared to GBM controls after 14 days, with a dose-dependent anti-GBM effect observed in MRI analyses. BA treatment improved hematological (WBC and PLT counts) and biochemical parameters (LDL-C, CREA, and ALP). Histopathological examination revealed a significant reduction in tumor diameter with 6.5 and 13 mg kg-1 BA. Immunohistochemical and immunofluorescence staining showed modulation of intracytoplasmic Ki67, cytoplasmic CMPK2, and GFAP expressions in tumor cells post-BA treatment. Additionally, BA did not increase micronuclei formations, indicating its non-genotoxic nature. In conclusion, targeting tumor suppressor networks with boron demonstrates significant therapeutic potential for GBM treatment.
- Journal
- MEDICAL ONCOLOGY
- Year
- 2025
- Volume
- 42
- Issue
- 2
- ISSN
- 1357-0560
- eISSN
- 1559-131X
- DOI
- 10.1007/s12032-025-02600-z
- WoS UID
- WOS:001400046200001