Marine Bio Research Team, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
Environ Toxicol Pharmacol. 2013 Jan;35(1):39-46. doi: 10.1016/j.etap.2012.10.002. Epub 2012 Oct 13.
The present study was designed to evaluate the molecular mechanisms of fucoxanthin against melanoma cell lines (B16F10 cells). Fucoxanthin reduced the proliferation of B16F10 cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G(0)/G(1) phase and apoptosis. Fucoxanthin-induced G(0)/G(1) arrest was associated with a marked decrease in the protein expressions of phosphorylated-Rb (retinoblastoma protein), cyclin D (1 and 2) and cyclin-dependent kinase (CDK) 4 and up-regulation of the protein levels of p15(INK4B) and p27(Kip1). Fucoxanthin-induced apoptosis was accompanied with the down-regulation of the protein levels of Bcl-xL, an inhibitor of apoptosis proteins (IAPs), resulting in a sequential activation of caspase-9, caspase-3, and PARP. Furthermore, the anti-tumor effect of fucoxanthin was assessed in vivo in Balb/c mice. Intraperitoneal administration of fucoxanthin significantly inhibited the growth of tumor mass in B16F10 cells implanted mice.
本研究旨在评估岩藻黄质对黑素瘤细胞系(B16F10 细胞)的分子机制。岩藻黄质呈剂量依赖性降低 B16F10 细胞的增殖,同时诱导细胞周期停滞于 G0/G1 期并引发细胞凋亡。岩藻黄质诱导的 G0/G1 期阻滞与磷酸化-Rb(视网膜母细胞瘤蛋白)、细胞周期蛋白 D(1 和 2)和细胞周期蛋白依赖性激酶(CDK)4 的蛋白表达明显减少以及 p15(INK4B)和 p27(Kip1)的蛋白水平上调有关。岩藻黄质诱导的细胞凋亡伴随着凋亡抑制蛋白(IAPs)的 Bcl-xL 蛋白水平下调,导致 caspase-9、caspase-3 和 PARP 的顺序激活。此外,还在 Balb/c 小鼠体内评估了岩藻黄质的抗肿瘤作用。腹腔内给予岩藻黄质可显著抑制植入 B16F10 细胞的小鼠肿瘤质量的生长。