Corchorusin-D (COR-D), isolated from Corchorus acutangulus, was reported to induce
apoptosis in leukemic cells. However, no studies concerning its activity on melanoma
cells have been reported. We have evaluated its in vitro anti-cancer activity on
melanoma cells (B16F10, SK-MEL-28, and A375). The results demonstrate that CORD
showed maximum inhibition of B16F10 cells in vitro. COR-D induced
mitochondrial dysfunction and altered the Bax/Bcl-2 ratio with down regulation of
pro-caspases 9 and activation of caspase 3 in B16F10 cells, triggering intrinsic pathway
of apoptosis. Moreover, it inhibited the in vivo B16F10 tumor growth and increased the
survival rate of mice. Greater number of Annexin V-FITC and propidium iodide (PI)-
positive tumor cells signified that COR-D induced apoptosis in vivo also. The reduction
in tumor growth is well correlated with decreased microvascular density of the tumor
cells in treated mice. In conclusion, this study reveals that COR-D-induced
mitochondrial dysfunction is responsible for the induction of apoptotic cell deat
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