Fucoidan inhibits the migration and proliferation of HT-29 human colon cancer cells via the phosphoinositide-3 kinase/Akt/mechanistic target of rapamycin pathways
- Yong‑Seok Han
- Jun Hee Lee
- Sang Hun Lee
Affiliations: Laboratory for Medical Science Research Institute, Soonchunhyang University, Seoul Hospital, Seoul 336‑745, Republic of Korea, 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
- Published online on: May 21, 2015 https://doi.org/10.3892/mmr.2015.3804
Copyright: © Han
et al. This is an open access article distributed under the
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Commons Attribution License [CC BY_NC 3.0].
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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.