Fucoidan from seaweed Fucus vesiculosus inhibits migration and invasion of human lung cancer cell via PI3K-Akt-mTOR pathways
Open accessAbstract
BACKGROUND: Recently there has been an increased interest in the pharmacologically active natural products associated with remedies of various kinds of diseases, including cancer. Fucoidan is a polysaccharide derived from brown seaweeds and has long been used as an ingredient in some dietary supplement products. Although fucoidan has been known to have anti-cancer activity, the anti-metastatic effects and its detailed mechanism of actions have been poorly understood. Therefore, the aims of this study were to demonstrate the anti-metastatic functions of fucoidan and its mechanism of action using A549, a highly metastatic human lung cancer cell line. METHODS AND PRINCIPAL FINDINGS: Fucoidan inhibits the growth of A549 cells at the concentration of 400 µg/ml. Fucoidan treatment of non-toxic dose (0-200 µg/ml) exhibits a concentration-dependent inhibitory effect on the invasion and migration of the cancer cell via decreasing its MMP-2 activity. To know the mechanism of these inhibitory effects, Western blotting was performed. Fucoidan treatment down-regulates extracellular signal-related kinase 1 and 2 (ERK1/2) and phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (PI3K-Akt-mTOR) pathways. Furthermore, fucoidan decreases the cytosolic and nuclear levels of Nuclear Factor-kappa B (p65). CONCLUSIONS/SIGNIFICANCE: The present study suggests that fucoidan exhibits anti-metastatic effect on A549 lung cancer cells via the down-regulation of ERK1/2 and Akt-mTOR as well as NF-kB signaling pathways. Hence, fucoidan can be considered as a potential therapeutic reagent against the metastasis of invasive human lung cancer cells.
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Fucoidan from F. vesiculosus inhibited migration and invasion of human lung cancer cells, decreasing cytosolic and nuclear levels of kappa-B nuclear factor.
“Fucoidan from F. vesiculosus inhibited the migration and the invasion of human lung cancer cells decreasing the cytosolic and nuclear levels of kappa-B nuclear factor [64].”
From Anticancer and Cancer Preventive Properties of Marine Polysaccharides: Some Results and Prospects (2013) · cites this paper as [64]
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- Authors
- Lee, H., Kim, J.-S., & Kim, E.
- Affiliations
- Gyeongsang National University (KR)
- Corresponding author
- Kim, Euikyung
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-11-30
- Volume
- 7
- Issue
- 11
- Pages
- e50624
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3511566
- OpenAlex
- W2092242450
- Cited by
- 191
- References
- 41
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 8 · 2023: 14 · 2022: 16 · 2021: 12 · 2020: 21 · 2019: 19 · 2018: 13 · 2017: 18 · 2016: 19 · 2015: 15 · 2014: 12 · 2013: 4
- FWCI
- 14.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Aquatic Science › Seaweed-derived Bioactive Compounds
- Life Sciences › Agricultural and Biological Sciences › Aquatic Science › Echinoderm biology and ecology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- fucoidan, Fucus vesiculosus, lung cancer, metastasis, cell migration, cell invasion, PI3K/AKT/mTOR pathway, ERK signaling, NF-κB, MMP-2, A549 cells, seaweed polysaccharides, antimetastatic activity
- MeSH terms
- Antineoplastic Agents, Cell Movement, Cell Nucleus, Humans, Lung Neoplasms, Neoplasm Invasiveness, Neoplasm Metastasis, Polysaccharides, Signal Transduction, Gene Expression Regulation, Neoplastic, NF-kappa B, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinase 1, Matrix Metalloproteinase 2, Active Transport, Cell Nucleus, Fucus, Cell Line, Tumor, Mitogen-Activated Protein Kinase 3, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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