title: Fucoidan inhibits the migration and proliferation of HT-29 human colon cancer cells via the phosphoinositide-3 kinase/Akt/mechanistic target of rapamycin pathways.
abstract: Fucoidan, a sulfated polysaccharide, has a variety of biological activities, including anti-cancer, anti-angiogenic and anti-inflammatory effects. However, the underlying mechanisms of fucoidan as an anti‑cancer agent remain to be elucidated. The present study examined the anti‑cancer effect of fucoidan on HT‑29 human colon cancer cells. The cell growth of HT29 cells was significantly decreased following treatment with fucoidan (200 µg/ml). In addition, fucoidan inhibited the migration of HT‑29 cells by decreasing the expression levels of matrix metalloproteinase‑2 in a dose‑dependent manner (0‑200 µg/ml). The underlying mechanism of these inhibitory effects included the downregulation of phosphoinositide 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) by treatment with fucoidan. Furthermore, fucoidan increased the expression of cleaved caspase‑3 and decreased cancer sphere formation. The present study suggested that fucoidan exerts an anti‑cancer effect on HT‑29 human colon cancer cells by downregulating the PI3K‑Akt‑mTOR signaling pathway. Therefore, fucoidan may be a potential therapeutic reagent against the growth of human colon cancer cells.
authors.affiliation: Laboratory for Medical Science Research Institute, Soonchunhyang University, Seoul Hospital, Seoul 336‑745, Republic of Korea.
authors.forename: Yong-Seok
authors.initials: YS
authors.lastname: Han
authors.affiliation: Department of Physiology, Laboratory for Vascular Medicine and Stem Cell Biology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, Gyeongsangnam-do 626‑870, Republic of Korea.
authors.forename: Jun Hee
authors.initials: JH
authors.lastname: Lee
authors.affiliation: Laboratory for Medical Science Research Institute, Soonchunhyang University, Seoul Hospital, Seoul 336‑745, Republic of Korea.
authors.forename: Sang Hun
authors.initials: SH
authors.lastname: Lee
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival; D004354:Drug Screening Assays, Antitumor; D019073:HT29 Cells; D006801:Humans; D020128:Inhibitory Concentration 50; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D011134:Polysaccharides / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D018874:Spheroids, Cellular / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D019869:Phosphatidylinositol 3-Kinases; D011134:Polysaccharides; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; C007789:fucoidan; C546842:MTOR protein, human