RESUMO
BACKGROUND/AIM: Glioblastoma multiforme is the most malignant type of glioma. Alpha-bisabolol is an essential oil reported as a potent cell death agent. In the present work, we evaluated the effect of alpha-bisabolol on ecto-5'-nucleotidase/CD73, the most well-characterized enzymatic source of adenosine, present in lipid rafts. MATERIALS AND METHODS: Glioma cells were treated with alpha-bisabolol and, in some experiments, pre-treated with an A3 antagonist. MTT assay (viability), malachite green method (ecto-5'-nucleotidase/CD73 activity) and quantitative polymerase chain reaction (qPCR) (A3 mRNA) were carried out. RESULTS: Alpha-bisabolol led to a decrease in C6 and U138-MG glioma cells viability, accompanied by an increase in ecto-5'-NT/CD73 activity. Pre-treatment with an A3 antagonist reverted the effect of α-bisabolol with an increase of mRNA expression of this receptor. CONCLUSION: Our data indicated the participation of ecto-5'-nucleotidase/CD73 and A3 receptor in the anti-proliferative effect of α-bisabolol on glioma cells.
Assuntos
5'-Nucleotidase/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Glioma/patologia , Receptor A3 de Adenosina/química , Sesquiterpenos/farmacologia , Animais , Western Blotting , Proliferação de Células/efeitos dos fármacos , Glioma/tratamento farmacológico , Glioma/metabolismo , Humanos , Sesquiterpenos Monocíclicos , RNA Mensageiro/genética , Ratos , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Células Tumorais CultivadasRESUMO
BACKGROUND/AIM: Despite recent progress in glioblastoma treatment, prognosis is still poor. Monastrol is a kinesin spindle protein (KSP) inhibitor and anticancer effects for this molecule have been reported. Here we describe the effect of LaSOM 65, a monastrol derivated compound, against glioma cell lines. MATERIALS AND METHODS: Cell counting, viability assay, lactate dehydrogenase (LDH) activity, cell-cycle analysis, immunofluorescence and organotypic hippocampal slice cultures were performed. RESULTS: LaSOM 65 reduced cell number and cell viability of gliomas cells, but did not cause arrest in the cell cycle at the G2/M phase. Measurement of LDH activity showed that LaSOM 65 induces necrosis after 48 h of treatment. CONCLUSION: LaSOM 65 appears to a be promising new molecule to treat glioblastoma since it promotes a decrease of cell growth and cell viability of glioma cells in vitro and does not induces the neurotoxic characteristics of the anti-mitotic drugs currently used.