Targeting glioblastoma with hybrid H ₃ R antagonists with piperidinylpropoxy and trimethoxychalcone motifs results in broad oncosuppressive effects

R expression levels. AR71 treatment decreased the invasion potential of cancer cells by 60-80% along with a decrease in MMP-2 release. In-depth immunocytochemical investigations revealed dose-dependent impairment of microtubule organisation after treatment with AR71. Consequently, tubulin polymerisation and cytokinesis failure led to a greater incidence of aneuploid cells and tripolar mitotic events. We also observed an increase in mitochondrial reactive oxygen species in cancer cells following exposure to AR71. As a result, the mitochondrial membrane potential decreased significantly. In summary, targeting dual molecules with AR71 may create favourable conditions for the selective and synergistic action of combined anticancer compounds against glioblastoma and neuroblastoma.