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Rom J Morphol Embryol ; 64(2): 173-180, 2023.
Article in English | MEDLINE | ID: mdl-37518874

ABSTRACT

The formation, proliferation, and evolution of glioblastoma (GB) are significantly influenced by pathological angiogenesis. This is supported by several growth factor receptors, such as the vascular endothelial growth factor receptor (VEGFR). In this experiment, we examined how the Food and Drug Administration (FDA) approved VEGFR blockers Sorafenib and Axitinib affect the viability of GB cells in vitro. Cells were cultivated in 96-well culture plates for the experiments, afterwards Sorafenib and Axitinib were administered at doses ranging from 0.3 µM to 80 µM. 2,5-Diphenyl-2H-tetrazolium bromide (MTT) assay was used to assess the impact of VEGFR inhibition on high-grade glioma (HGG) cell lines. To observe the morphological changes in cell shape, we used a 10× magnification microscopy. Our results showed that both Axitinib and Sorafenib retarded GB1B culture proliferation in a dose- and time-dependent manner in comparison to control cohorts that had not received any treatment. The half maximal inhibitory concentration (IC50) value for Axitinib was 3.5839 µM after three days of drug administration and 2.2133 µM after seven days of drug administration. The IC50 value for Sorafenib was 3.5152 µM after three days of drug administration and 1.6846 µM after seven days of drug administration. After the treatment with Axitinib or Sorafenib, very few cells became rounded and detached from the support, others remained adherent to the culture substrate, but acquired a larger, flatter shape. Our results indicate that VEGFR might serve as a key target in the treatment of GB. Although it is known that in vitro some drugs block the VEGFR more potently, clinical evidence is required to show whether this actually translates to better clinical outcomes.


Subject(s)
Antineoplastic Agents , Glioblastoma , Humans , Axitinib/pharmacology , Sorafenib/pharmacology , Glioblastoma/drug therapy , Cell Survival , Vascular Endothelial Growth Factor A/metabolism , Indazoles/pharmacology , Indazoles/therapeutic use , Antineoplastic Agents/pharmacology , Antineoplastic Agents/therapeutic use
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