Effects of crude water-soluble extract of Momordica charantia on viability, caspase activity, cytochrome-c release and on cytosolic calcium levels in different cancer cell lines

Prior to the availability of chemotherapeutic agents, dietary measures, including traditional medicines derived from plants, were the major forms of cancer treatment. One such plant is Momordica charantia (Family: Cucurbitaceae), whose fruit is known as corilla or bitter gourd/melon. M. charantia possesses anti-carcinogenic properties and it can modulate its effect via xenobiotic metabolism and oxidative stress. This study investigated the anti-cancer effect of an active water-soluble extract (s) of M. charantia on cell viability and its cellular mechanism(s) of action in inducing cell death. The fruit was washed and cut in to small pieces, liquidised in deionised water using a blender and subsequently, dried using a rota evaporator and oven. Both time course (800 μg/ml) and dosedependent (200 μg/ml800 μg/ml) experiments were performed treating six different cancer cell lines, namely 1321N1, Gos-3, U87-MG, Sk Mel, Corl -23, Weri Rb-1 and normal L6 muscle cell line with the crude fruit extract for 24-48 hours at 37 °C. Cell viability was measured using the MTT assay. The results show that the crude water soluble extract of M. charantia can evoke both time-course (800 μg/ml) and dose-dependent (200 μg/ml 800 μg/ml) decreases in cell viability (cell death) with maximal increases in cell death employing 800 μg/ml over a period of 24 hours following incubation. The results of this study have also shown that the crude water-soluble extract of M. charantia (800 μg/ml) can elicit marked and significant (p < 0.05) increases in the activities of caspase 3 and caspase 9 in all the cell lines. The crude water soluble extract of M. charantia can stimulate the release of cytochrome-c and elevated intracellular free calcium concentrations [Ca]i in the different cancer cell lines compared to untreated cell lines. These results clearly show that M. charantia is exerting its anticancer effect via an insult to the mitochondria resulting in apoptosis, calcium overloading and subsequently, cell death.