Abstract
Tea Tree oil (TTO), the essential oil from the Australian native Melaleuca alternifolia has demonstrated a variety of beneficial efficacies including antimicrobial, antifungal, antiviral and anti-inflammatory. This report discusses data obtained on the in vitro activity of TTO on human glioblastoma cells U87MG. Cell viability was examined by 2-(4,5-dimethyl-2-thiazolyl)-3,5-diphenyl-2H-tetrazolium bromide MTT assay. Growth was investigated by incubating cells with various concentrations of TTO (0.025 and 0.05 %) for 24, 48 or 72 h and daily cell count. Cell cycle and apoptosis assay were assessed by flow citometry. TTO decreased cell viability in a dose and time-dependent manner. . The cell cycle distribution showed that TTO enhanced the accumulation of the cells in G0/G1 phase. The analysis by Western blot of protein related to cell cycle (CDK2 and p27), cell apoptosis (caspase 6 and 8), necrosis (TNFR1 and RIP1) demonstrated that TTO induces U87MG growth inhibition by more synergic mechanisms: necrosis, low level apoptosis and cell cycle arrest. TTO induces also in vivo glioblastoma tumor growth inhibition in a murine subcutaneous model. Key words: Brain cancer, tea tree oil, terpinol, glioblastoma, natural drug, adjuvant chemotherapy, temozolomide, apoptosis, cell cycle.
Highlights
Glioblastoma (GBM) is the most common primary malignant form of brain cancer, with a median survival of 7-15 months from the time of diagnosis
Tea Tree oil (TTO) inhibits the viability of U87MG glioblastoma cells
Our results indicated that TTO triggers cell cycle arrest in the G0 / G1 phase in a time and dose dependent manner showing a significant effect after 72 h
Summary
Glioblastoma (GBM) is the most common primary malignant form of brain cancer, with a median survival of 7-15 months from the time of diagnosis. Hallmarks of the aggressive cancer include extensive infiltration and strong vascular proliferation into the surrounding brain parenchyma (Wei et al, 2014; Kim et al, 2015; VanTellingen et al, 2015). The presence of cancer stem cells, was able to proliferate and generate glial neoplastic cell, contribute to the unfavourable prognosis of GBM patients (Surawicz et al, 1998).
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