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Fucoidan Treatment Leads to Attenuated Growth Factor Signaling and Reduced Proliferation in Neuroblastoma Cells
Niklas Weber1, Nina Sophie Pommert1, Meike Kaehler1
1Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Background/Aim:
Brown algae-derived sulfated polysaccharides, termed as fucoidans, are pharmacologically active substances with pleiotropic anticancer properties, but without known toxicity. In neuroblastoma, an aggressive malignancy with a heterogeneous biological basis, multimodal therapeutic approaches are mandatory for high-risk patients, but these are associated with a problematic safety profile. The present study aimed to examine fucoidan-mediated effects in human neuroblastoma cells to assess their putative tumor-suppressive potential.
Materials And Methods:
In Kelly or SH-SY5Y cells, viability was quantified using cell fitness assays. Expression was analyzed using quantitative PCR and the regulation or phosphorylation of proteins using enzyme-linked immunoabsorbent assays (ELISA) or Western blots.
Results:
In Kelly and SH-SY5Y cells, treatment with fucoidans from Fucus vesiculosus (F.v.) or Saccharina latissima (S.l.) for 3 days did not induce cell death, but significantly reduced proliferation (p<0.001), which was associated with attenuated signaling of hepatocyte growth factor (HGF), insulin-like growth factor 2 (IGF2) and vascular endothelial growth factor (VEGF). Despite cell type- and fucoidan-specific differences, co-administration of the fucoidans from F.v. or S.l. and specific receptor inhibitors of HGF (tepotinib), IGF2 (linsitinib) or VEGF (cediranib), distinctly reduced cell viability compared to inhibitor treatment alone in both cell lines (p<0.001). Interestingly, the fucoidan from S.l. also enhanced the antitumor effect of the endothelial growth factor (EGF) receptor inhibitor erlotinib in Kelly and SH-SY5Y cells, although endogenous EGF was not detectable.
Conclusion:
Fucoidan treatment decreased proliferation in neuroblastoma cells by interfering with the signal transduction of HGF, IGF2, and VEGF, which substantially increased cellular susceptibility to specific growth factor receptor inhibitors.
Insights
Fucoidans from brown algae inhibit neuroblastoma cell proliferation by disrupting growth factor signaling pathways. This enhances the effectiveness of targeted cancer therapies, offering a safer treatment approach.
Area of Science:
- Marine biotechnology
- Cancer biology
- Pharmacology
Background:
- Fucoidans, sulfated polysaccharides from brown algae, exhibit anticancer properties without known toxicity.
- Neuroblastoma, a high-risk pediatric cancer, requires multimodal therapies with significant side effects.
- Investigating fucoidans offers a potential strategy to improve neuroblastoma treatment safety and efficacy.
Purpose of the Study:
- To evaluate the tumor-suppressive potential of fucoidans in human neuroblastoma cells.
- To determine the impact of fucoidan on key signaling pathways involved in neuroblastoma growth.
- To assess the synergistic effects of fucoidans with targeted cancer therapies.
Main Methods:
- Human neuroblastoma cell lines (Kelly, SH-SY5Y) were treated with fucoidans from *Fucus vesiculosus* and *Saccharina latissima*.
- Cell viability and proliferation were assessed using cell fitness assays.
- Protein expression and phosphorylation were analyzed via ELISA and Western blotting; quantitative PCR was used for gene expression analysis.
Main Results:
- Fucoidan treatment significantly reduced neuroblastoma cell proliferation without inducing cell death.
- Fucoidans attenuated signaling pathways of hepatocyte growth factor (HGF), insulin-like growth factor 2 (IGF2), and vascular endothelial growth factor (VEGF).
- Co-administration of fucoidans with specific receptor inhibitors (tepotinib, linsitinib, cediranib) significantly reduced cell viability, outperforming inhibitor treatment alone.
Conclusions:
- Fucoidan treatment inhibits neuroblastoma cell proliferation by interfering with HGF, IGF2, and VEGF signaling.
- Fucoidans enhance the efficacy of targeted growth factor receptor inhibitors, suggesting a role in combination cancer therapy.
- Fucoidans represent a promising, non-toxic agent for improving neuroblastoma treatment strategies.
