Many reports indicate that the antitumor activates of Fucoidan have been observed in vivo and in vitro. The mechanism underlying the antitumor activities of Fucoidan has been reported to include the induction of apoptosis, suppression of angiogenesis, and activation of cell-mediated immunity. In particular, Fucoidan increases the activity of natural killer cells in vivo. Fucoidan promotes human monocytes’ maturation to dendritic cells and stimulates interleukin (IL) release -12 and interferon-γ in vitro. Previous reports have indicated that Fucoidan is a beneficial antitumor agent; however, almost all information describing the antitumor effects of Fucoidan in vivo has evaluated fucoidan administration intraperitoneally intravenously or by regional injection into tumor tissues. Few reports have investigated the beneficial effects of oral administration of Fucoidan in mouse or rat tumor models.

The study “Effects of Oral Administration of Fucoidan Extracted from Cladosiphon okamuranus on Tumor Growth and Survival Time in a Tumor-Bering Mouse Model” examined the effects of oral administration and different fucoidan molecular weights on tumor growth and survival time by Kazuo Azuma et al.

The materials used included low-molecular-weight fucoidan (LMWF: 6.5~40 kDa), intermediate-molecular-weight fucoidan (IMWF: 110~138 kDa) and high-molecular-weight fucoidan (HmWF: 00~330 kDa). After fed food with 5%(w/w) fucoidan preparation for 28 days, Following the oral administration of Fucoidan in a colon 26 tumor-bearing mice mode, and from the 14 days of cancer transplantation, we observed tumor weight and survival days. As for the result, the tumor weights were decreased in each group comparing the control group, especially significantly decreased in the intermediate-molecular-weight fucoidan group (IMWF) (Fig.1). At that time, IMWF inhibited cancer cells’ proliferation and observed a slight induction of apoptosis.  The mice’s survival times in every fucoidan-fed mice were prolonged, especially the mice’s survival time in the LMWF and HMWF group were significantly increased compared to that observed in control; group (Fig 2).

The mouse who fed HMWF for 70days increased the population of the NK cells in the mouse spleen. Since the antitumor effect due to Fucoidan feeding was not observed in the mouse defected in myeloid differentiation primary response protein MyD88 involved activation of the innate immune response such as dendritic cells that the oral administration of HMWF was shown to antitumor effect through activation of the immune system. To understand the mechanism of the antitumor activities exhibited by IMWF and LMWF, further studies must be conducted.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497027/