There are numerous research studies on PubMed that show Fucoidan’s multi-faceted anti-cancer activity across a wide range of tumor types:
In recent research, fucoidan was shown to inhibit the growth of a colon cancer cell line via inhibition of T-cell originated protein kinase (TOPK). In this study, fucoidan was also orally administered to mice and found to suppress the growth of human colorectal tumors through the same pathway. Results show the potential for fucoidan to be used as a complementary therapy to improve the effectiveness of current cancer treatments. Fucoidan has also been shown to induce DNA damage and cause cell cycle arrest in the first growth phase of a HCT116 human colon cancer cell line. This action disrupts the ability for the cancer cells to divide and spread.
In a lung cancer mouse model, fucoidan down-regulated the expression of a number of key markers associated with tumor development, spread of proliferation. These markers included matrix and metalloproteinases, NF-Κβ and vascular endothelial growth factor. The orally ingested fucoidan was shown to reduce lung masses and lessen weight loss.
In an in vitro study, fucoidan inhibited the growth of liver cancer cells through the AMPK-associated suppression of fatty acid synthesis and cell cycle G1/S transition. In further in vitro research, fucoidan increased the activity of tumor suppressor proteins p53 and p38 MAPK, which directly inhibits the proliferation of hepatic tumor cells and induces apoptosis.
Fucoidan reduced the growth of oral cancer cells and caused cell death in an in vitro study of mucoepidermoid carcinoma, a type of oral cancer. In this research, fucoidan decreased cell proliferation and induced caspase-dependent apoptosis via down-regulation of the extracellular signal-regulated kinase ERK1/2.
Extensive research demonstrates the effects of fucoidan on breast cancer in animal models. Fucoidan has been shown to significantly improve the effectiveness of tamoxifen, a common chemotherapy used in breast cancer. In a mouse model, orally ingested fucoidan reduced breast cancer tumor growth by up to an additional 26% when taken alongside tamoxifen.
Fucoidan has been shown to induce cell death in an in vitro study of PC-3 human prostate cancer cells. In the study, fucoidan was shown to activate apoptosis through the use of both intrinsic and extrinsic pathways. Fucoidan has also been found to inhibit growth and induce apoptosis in DU145 human prostate cancer cells involving the PI3K/Akt signaling pathway.
Fucoidan has been shown to decrease the growth of a TOC-112D human ovarian cancer cell line. In a mouse model, the ingestion of fucoidan decreased the growth of this tumor line by up to 33%.
Fucoidan has been shown to reduce the growth of HeLa human cervical cancer cell line. Ingestion of fucoidan was found to decrease the growth of this tumor line by up to 70% in a mouse model.
Fucoidan decreased the ability for pancreatic cancer cells to secrete matrix-degrading enzymes required to metastases and spread in an in vitro model. In addition, f ucoidan was shown to interfere with the binding of chemokines to the cellular receptor CXCR4. Inhibition of CXCR4 has been shown in an animal model to reduce pancreatic tumor growth and metastases. Fucoidan also demonstrated potential to reduce the effects of acute pancreatitis due to its ability to block selectins.