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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.
AuthorsYong-Seok Han, Jun Hee Lee, Sang Hun Lee
JournalMolecular medicine reports (Mol Med Rep) Vol. 12 Issue 3 Pg. 3446-3452 (Sep 2015) ISSN: 1791-3004 [Electronic] Greece
PMID25998232 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Polysaccharides
  • fucoidan
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
Topics
  • Antineoplastic Agents (pharmacology)
  • Cell Movement (drug effects)
  • Cell Proliferation (drug effects)
  • Cell Survival
  • Drug Screening Assays, Antitumor
  • HT29 Cells
  • Humans
  • Inhibitory Concentration 50
  • Phosphatidylinositol 3-Kinases (metabolism)
  • Polysaccharides (pharmacology)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Signal Transduction (drug effects)
  • Spheroids, Cellular (drug effects)
  • TOR Serine-Threonine Kinases (metabolism)

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