Yoshiko Satomi, Hoyoku Nishino
Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
In Vivo. 2007 Mar-Apr;21(2):305-9.
Although the antitumor effects of fucoxanthin are known, the precise mechanism of action has yet to be elucidated.
HepG2 and DU145 cells were used for these investigations. The effect of fucoxanthin on gene expression was assayed using a DNA microarray system. Northern blot and/or quantitative RT-PCR were carried out to confirm any changes in gene expression. The effect of fucoxanthin on cell cycle progression was analyzed using flow cytometry. RNA interference experiments were employed for the GADD45 gene.
Fucoxanthin markedly induced GADD45A, a cell cycle-related gene, in HepG2 and DU145 cells. Concomitant G1 arrest, but not apoptosis, was observed in both cell types following treatment with fucoxanthin. The introduction of siRNA against GADD45A partially perturbed the induction of Gi arrest by fucoxanthin in both cell types.
Fucoxanthin induced G1 arrest in HepG2 and DU145 cells. GADD45A may be involved in fucoxanthin-induced G1 arrest.
尽管岩藻黄质的抗肿瘤作用已为人所知,但其确切作用机制尚未阐明。
本研究采用HepG2和DU145细胞。利用DNA微阵列系统检测岩藻黄质对基因表达的影响。进行Northern印迹和/或定量RT-PCR以确认基因表达的任何变化。使用流式细胞术分析岩藻黄质对细胞周期进程的影响。对GADD45基因进行RNA干扰实验。
岩藻黄质在HepG2和DU145细胞中显著诱导细胞周期相关基因GADD45A。在用岩藻黄质处理后,两种细胞类型均观察到伴随的G1期阻滞,但未观察到凋亡。针对GADD45A的siRNA的导入在两种细胞类型中部分干扰了岩藻黄质诱导的G1期阻滞。
岩藻黄质在HepG2和DU145细胞中诱导G1期阻滞。GADD45A可能参与岩藻黄质诱导的G1期阻滞。