Fucoidan induces apoptosis of HepG2 cells by down-regulating p-Stat3

Summary： 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, Cyelin B 1 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.     

水杨酸衍生物抗乳腺癌的研究进展

目前的研究表明,阿司匹林、水杨酸钠、水杨酸铜等水杨酸衍生物具有抑制乳腺癌生长的作用。其中,阿司匹林作为水杨酸衍生物的代表,其抗肿瘤分子机制研究颇多,主要包括阿司匹林可降低COX酶活性以及影响NF-κB等多种重要蛋白的表达。为进一步研究水杨酸衍生物在乳腺癌治疗中的作用,本文对水杨酸衍生物抑制乳腺癌细胞增殖及其作用机制的进展进行综述。