Anti-tumor effects of a carotenoid isolated from brown algae and analysis of related signaling pathway

Abstract

There are various species of marine algae in Jeju Island, Korea. Useful secondary metabolites are obtained from marine algae. Several recent reports have indicated that fucoxanthin, a carotenoid found in seaweed, inhibits tumor cell growth by modulating the expression of cell cycle-regulatory and apoptosis-related genes. However, information concerning its ability to induce cell cycle arrest and apoptosis in melanoma is lacking. Therefore, the principal objective of this study was to explore in more detail the mechanisms underlying fucoxanthin induced apoptosis in HL-60 and B16F10 cells. Our data reveal that HL-60 cells are highly sensitive to growth inhibition and apoptosis induction by fucoxanthin. Fucoxanthin-induced apoptosis is associated with Bcl-xL signaling pathways, which are mediated by ROS generation. fucoxanthin has ntiproliferative effects on B16F10 cells by inducing apoptosis and cell-cycle arrest. It increased the proportion of cells in the G1 phase of the cell cycle, which was associated with decreased cyclin D1 and D2, and CDK4 expressions and increased p15INK4B and p27Kip1 expressions. Fucoxanthin- induced apoptosis might be related to caspase-3 and -9 activation and the downregulation of Bcl-xL and IAP expressions. Taken together, the data presented in this study provide important insights into this cell cycle-based therapeutic strategy and form a strong basis for the dwth by modulating the expression of cell cycle-regulatory and apoptosis-related genes. However, information concerning its ability to induce cell cycle arrest and apoptosis in melanoma is lacking. Therefore, the principal objective of this study was to explore in more detail the mechanisms underlying fucoxanthin induced apoptosis in HL-60 and B16F10 cells. Our data reveal that HL-60 cells are highly sensitive to growth inhibition and apoptosis induction by fucoxanthin. Fucoxanthin-induced apoptosis is associated with Bcl-xL signaling pathways, which are mediated by ROS generation.