Roshan Sadia, Liu Yun-Yi, Banafa Amal, Chen Hui-Jie, Li Ke-Xiu, Yang Guang-Xiao, He Guang-Yuan, Chen Ming-Jie
The Genetic Engineering International Cooperation Base of Chinese Ministry of Science and Technology, Key Laboratory of Molecular Biophysics of Chinese Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China.
J Huazhong Univ Sci Technolog Med Sci. 2014 Jun;34(3):330-336. doi: 10.1007/s11596-014-1278-0. Epub 2014 Jun 18.
Fucoidan is one of the main bioactive components of polysaccharides. The current study was focused on the anti-tumor effects of fucoidan on human heptoma cell line HepG2 and the possible mechanisms. Fucoidan treatment resulted in cell cycle arrest and apoptosis of HepG2 cells in a dose-dependent manner detected by MTT assay, flow cytometry and fluorescent microscopy. The results of flow cytometric analysis revealed that fucoidan induced G2/M arrest in the cell cycle progression. Hoechst 33258 and Annexin V/PI staining results showed that the apoptotic cell number was increased, which was associated with a dose-dependent up-regulation of Bax and down-regulation of Bcl-2 and p-Stat3. In parallel, the up-regulation of p53 and the increase in reactive oxygen species were also observed, which may play important roles in the inhibition of HepG2 growth by fucoidan. In the meantime, Cyclin B1 and CDK1 were down-regulated by fucoidan treatment. Down-regulation of p-Stat3 by fucoidan resulted in apoptosis and an increase in ROS in response to fucoidan exposure. We therefore concluded that fucoidan induces apoptosis through the down-regulation of p-Stat3. These results suggest that fucoidan may be used as a novel anti-cancer agent for hepatocarcinoma.
岩藻依聚糖是多糖的主要生物活性成分之一。当前的研究聚焦于岩藻依聚糖对人肝癌细胞系HepG2的抗肿瘤作用及其可能的机制。通过MTT法、流式细胞术和荧光显微镜检测发现，岩藻依聚糖处理以剂量依赖的方式导致HepG2细胞的细胞周期停滞和凋亡。流式细胞术分析结果显示，岩藻依聚糖在细胞周期进程中诱导G2/M期停滞。Hoechst 33258和Annexin V/PI染色结果表明凋亡细胞数量增加，这与Bax的剂量依赖性上调以及Bcl-2和p-Stat3的下调有关。同时，还观察到p53的上调和活性氧的增加，它们可能在岩藻依聚糖抑制HepG2生长中发挥重要作用。与此同时，岩藻依聚糖处理使细胞周期蛋白B1和细胞周期蛋白依赖性激酶1下调。岩藻依聚糖对p-Stat3的下调导致凋亡以及对岩藻依聚糖暴露产生的活性氧增加。因此，我们得出结论，岩藻依聚糖通过下调p-Stat3诱导凋亡。这些结果表明岩藻依聚糖可能用作肝癌的新型抗癌剂。
