METHODS: M. cochinchinensis aril from 44 different samples in Australia, Thailand and Vietnam were extracted using different solvents and tested for its anticancer potential. Anticancer activity of M. cochinchinensis aril on breast cancer (MCF7 and BT474) and melanoma (MM418C1 and D24) cells were compared to control fibroblasts (NHDF). The cytotoxicity of the cells following treatment with the aril extract was determined using CCK-8 assay. Biochemical and morphological changes were analysed using flow cytometry, confocal and transmission electron microscopy to determine the mechanism of cell death.
RESULTS: The water extract from the aril of M. cochinchinensis elicited significantly higher cytotoxicity towards breast cancer and melanoma cells than the HAE extract. The IC50 concentration for the crude water extract ranged from 0.49 to 0.73 mg/mL and induced both apoptotic and necrotic cell death in a dose- and time-dependant manner with typical biochemical and morphological characteristics. The greatest cytotoxicity was observed from Northern Vietnam samples which caused 70 and 50% melanoma and breast cancer cell death, respectively.
CONCLUSIONS: The water extract of M. cochinchinensis aril caused significant apoptosis and necrosis of breast cancer and melanoma cells, with varieties from Northern Vietnam possessing superior activity. This highlights the potential of this fruit in the development of novel anticancer agents against such tumours, with specific regions on where to collect the best variety and extraction solvent for optimum activity.
METHODS: The cytotoxicity of E. cuneatum extract was evaluated by both MTS and LDH assays. Genotoxicity study on E. cuneatum extract was assessed by the single cell gel electrophoresis (comet assay). The protective effect of E. cuneatum against menadione-induced cytotoxicity was also investigated.
RESULTS: Results from this study showed that E. cuneatum extract exhibited cytotoxic activities towards the cells with IC50 value of (125±12) and (125±14) μg/mL for HepG2 and WRL68 cells respectively, after 72 h incubation period as determined by MTS assay. LDH leakage was detected at (251±19) and (199.5±12.0) μg/mL for HepG2 and WRL68 respectively. Genotoxicity study results showed that treatment with E. cuneatum up to 1 mg/mL did not cause obvious DNA damage in WRL68 and HepG2 cells. Addition of E. cunaetum did not show significant protection towards menadione in WRL68 and HepG2 Cells.
CONCLUSIONS: E. cuneatum standardized aqueous extract might be developed in order to establish new pharmacological possibilities for its application.