Fucoidan Inhibited 4T1 Mouse Breast Cancer Cell Growth In Vivo and In Vitro Via Downregulation of Wnt/β-Catenin Signaling

Abstract

Fucoidan is a sulfated polysaccharide derived from brown algae and is known to possess anticancer properties. However, the relationship between fucoidan and β-catenin, one of the key components of the Wnt signaling pathway, in mouse breast cancer remains poorly characterized. In this study, mouse breast cancer cells (4T1) were exposed to fucoidan to investigate the relationship between fucoidan and the Wnt/β-catenin signaling pathway in vivo and in vitro. We found that fucoidan significantly inhibited cell growth, increased cell death, and induced G1 cell cycle arrest in 4T1 cells. Fucoidan also reduced β-catenin expression and T cell factor/lymphoid-enhancing factor reporter activity. Furthermore, fucoidan downregulated the expression of downstream target genes such as c-myc, cyclin D1, and survivin. Intraperitoneal injection of fucoidan in tumor-bearing mice reduced the tumor volume and weight. Fucoidan induced aberrant downregulation of β-catenin in tumor tissues with a significant increase in apoptosis. Thus, our data suggested that fucoidan exerts its anticancer activity through downregulation of Wnt/β-catenin signaling. Fucoidan may be an effective therapy for the chemoprevention and treatment of mouse breast cancer.

ACKNOWLEDGMENTS

We thank Xihe Xie and Quan Li for their helpful comments and discussion on this study. This work was supported by a Grant from the Research Foundation (2010) of Qingdao Municipal Science and Technology Bureau.