METHODOLOGY/PRINCIPAL FINDINGS: The hexane extract of C. cassia demonstrated high anti-proliferative activity against MCF-7 and MDA-MB-231 cells (IC50, 34 ± 3.52 and 32.42 ± 0.37 μg/ml, respectively). Oxidative stress due to disruption of antioxidant enzyme (SOD, GPx and CAT) activity is suggested as the probable cause for apoptosis initiation. Though the main apoptosis pathway in both cell lines was found to be through caspase-8 activation, caspase-9 was also activated in MDA-MB-231 cells but suppressed in MCF-7 cells. Gene expression studies revealed that AKT1, the caspase-9 suppressor, was up-regulated in MCF-7 cells while down-regulated in MDA-MB-231 cells. Although, AKT1 protein expression in both cell lines was down-regulated, a steady increase in MCF-7 cells was observed after a sharp decrease of suppression of AKT1. Trans-cinnamaldehyde and coumarin were isolated and identified and found to be mainly responsible for the observed anti-proliferative activity of CE (Cinnamomum cassia).
CONCLUSION: Activation of caspase-8 is reported for the first time to be involved as the main apoptosis pathway in breast cancer cell lines upon treatment with C. cassia. The double effects of C. cassia on AKT1 gene expression in MCF-7 cells is reported for the first time in this study.
METHODS: The cytotoxic activity of the hexane and ethyl acetate extracts of Curcuma mangga rhizomes against human colorectal adenocarcinoma cell lines (HT29) was determined by using the SRB assay.
RESULTS: The ethyl acetate extract showed a higher cytotoxic effect compared to the hexane extract. Morphological changes of the HT29 cells such as cell shrinkage, membrane blebbling and formation of apoptotic bodies while changes in nuclear morphology like chromatin condensation and nuclear fragmentation were observed. Further evidence of apoptosis in HT29 cells was further supported by the externalization of phosphatidylserine which indicate early sign of apoptosis.
CONCLUSIONS: The early sign of apoptosis is consistent with the cell cycle arrest at the G0/G1 checkpoint which suggests that the changes on the cell cycle lead to the induction of apoptosis in HT29.