Cancer:
Lymphoma, prostate, hepatocellular carcinoma, breast, colorectal
Action: Chemotherapy protective
Fucoidan is a ulphated polysaccharide found in brown seaweed, including Sargassum thunbergii [(Mertens ex Roth) Kuntze] and Fucus vesiculosus (L.).
Lymphoma
Fucoidan, a sulfated polysaccharide in brown seaweed, was found to inhibit proliferation and induce apoptosis in human lymphoma HS-Sultan cell lines. Fucoidan-induced apoptosis was accompanied by the activation of caspase-3 and was partially prevented by pre-treatment with a pan-caspase inhibitor, z-VAD-FMK. The neutralizing antibody, Dreg56, against human l-selectin, did not prevent the inhibitory effect of fucoidan on the proliferation of IM9 and MOLT4 cells, both of which express l-selectin; thus it is possible fucoidan induced apoptosis through different receptors. These results demonstrate that fucoidan has direct anti-cancer effects on human HS-Sultan cells through caspase and ERK pathways (Aisa et al., 2005).
Colorectal Cancer; Chemotherapy
A total of 20 patients with unresectable advanced or recurrent colorectal cancer scheduled to undergo treatment with FOLFOX or FOLFIRI were randomly allocated into a fucoidan treatment group (n=10) and a control group without fucoidan treatment (n=10). Results showed that fucoidan regulated the occurrence of fatigue during chemotherapy. Chemotherapy with fucoidan was continued for a longer period than chemotherapy without fucoidan. Additionally, the survival of patients with fucoidan treatment was longer than that of patients without fucoidan, although the difference was not significant.
Thus, fucoidan may enable the continuous administration of chemotherapeutic drugs for patients with unresectable advanced or recurrent colorectal cancer, and as a result, the prognosis of such patients is prolonged (Ikeguchi et al., 2011).
Prostate Cancer
Fucoidan obtained from Undaria pinnatifida induced the apoptosis of PC-3 cells by activating both intrinsic and extrinsic pathways. The induction of apoptosis was accompanied by the activation of extracellular signal-regulated kinase mitogen-activated protein kinase (ERK1/2 MAPK) and the inactivation of p38 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt. In addition, fucoidan also induced the up-regulation of p21Cip1/Waf and down-regulation of E2F-1 cell-cycle-related proteins. Furthermore, in the Wnt/β-catenin pathway, fucoidan activated GSK-3β that resulted in the decrease of β-catenin level, followed by the decrease of c-myc and cyclin D1 expressions, target genes of β-catenin in PC-3 cells. The data support that fucoidan might have potential for the treatment of prostate cancer (Boo et al., 2013).
Hepatocellular Carcinoma
Fucoidan isolated from U. pinnatifida induced apoptosis in human hepatocellular carcinoma SMMC-7721 cells via the ROS-mediated mitochondrial pathway. SMMC-7721 cells exposed to fucoidan displayed growth inhibition and several typical features of apoptotic cells, such as chromatin condensation and marginalization, and a decrease in the number of mitochondria, and in mitochondrial swelling and vacuolation (Yang et al., 2013).
Breast Cancer
Fucoidan exerts its anti-cancer activity through down-regulation of Wnt/β-catenin signaling. Fucoidan may be an effective therapy for the chemoprevention and treatment of mouse breast cancer. Fucoidan significantly inhibited cell growth, increased cell death, and induced G1 cell- cycle arrest in breast cancer 4T1 cells. Fucoidan also reduced β-catenin expression and T cell factor/lymphoid-enhancing factor reporter activity. Furthermore, fucoidan down-regulated the expression of downstream target genes such as c-myc, cyclin D1, and survivin (Xue et al., 2013).
References