Inhibition of lewis lung cancer cell growth and migration by fucoidan

Research paper by Yong-seok Han, Jun Hee Lee, Hun Soo Chang, Sang Hun Lee

Indexed on: 23 Oct '14Published on: 23 Oct '14Published in: Molecular & Cellular Toxicology


Fucoidan has known anticancer activity in various cancer cell types. In the present study, the anticancer activity of fucoidan in Lewis lung cancer cells (LLC) and the underlying mechanism of action were investigated. To explore the mechanism of these anticancer effects, the phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) and the apoptosis signaling pathway were examined by western blot analysis. LLC growth was significantly inhibited following treatment with fucoidan (50 μg/mL). Moreover, fucoidan inhibited the invasion and migration of LLCs by regulating matrix metallopeptidase-2 expression. Fucoidan induced down regulation of the PI3K-Akt-mTOR pathway in LLC and caused significant apoptosis through increased mTOR-associated cleaved-caspase-3 expression. Collectively, these findings identify the regulation of PI3K-Akt-mTOR signaling, MMP-2 expression, and caspase-3 activation by fucoidan as a critical anti-cancer mechanism in lung cancer cells, suggesting that fucoidan is a potential therapeutic agent for treating lung cancer.