Induction of apoptosis in MCF-7 via the Caspase pathway by longilactone from Eurycoma longifolia Jack

Abstract

The effects of longilactone isolated from Eurycoma longifolia Jack were studied in human breast cancer cell line MCF-7. The research aim was to investigate the possible molecular mechanism of action of longilactone on MCF-7. The SRB assay showed that longilactone exerts a strong cytotoxic activity on MCF-7 with an IC50 of 0.53 ± 0.19 µg/ml. Hoechst 33342 staining assay and TEM analysis showed that longilactone induced apoptosis in MCF-7 as evidenced by nuclear condensation, fragmentation and margination; apoptosis induction occurred in a time-dependent manner. Western blot analysis indicated that longilactone activated the caspase-7,-8 and poly (ADP-ribose) polymerase, but failed to activate caspase-9. The basal levels of Bcl-2 and Bax were also not influenced by longilactone. Results indicate that longilactone induced apoptosis in MCF-7 via an extrinsic pathway, but not through an intrinsic pathway. We conclude that longilactone is a promising cytotoxic chemotherapeutic agent for treating breast cancer after further evaluation. Key words: Longilactone, Eurycoma longifolia, MCF-7, apoptosis, caspase.