Description: <b>Fucoidan</b> is found in brown algae. Extracted from the seaweed species Fucus vesiculosus, Cladosiphon okamuranus, Laminaria japonica and Undaria pinnatifida.<br>
In oncology research, fucoidan is most consistently described as an immunomodulatory and anti-angiogenic compound with additional pro-apoptotic and anti-metastatic effects in preclinical models. Mechanistically, fucoidan has been reported to suppress NF-κB and PI3K/AKT signaling, reduce VEGF-mediated angiogenesis, inhibit tumor cell adhesion and invasion, and promote apoptosis through caspase activation and mitochondrial pathways. It may also enhance NK cell and macrophage activity, contributing to anti-tumor immune responses. Effects vary substantially depending on molecular weight, sulfation pattern, and source species. Human clinical data remain limited, and many anticancer claims are derived from in vitro and animal studies.<br>
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<h3>Cancer Pathway Table: Fucoidan</h3>
<!-- Cancer Pathway Table: Fucoidan -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer / Tumor Context</th>
<th>Normal Tissue Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>Immune activation (NK cells / macrophages)</td>
<td>NK activity ↑; macrophage activation ↑ (reported)</td>
<td>Immune surveillance support</td>
<td>R, G</td>
<td>Immunostimulatory</td>
<td>One of the most consistent themes; fucoidan enhances innate immune responses in tumor-bearing animal models.</td>
</tr>
<tr>
<td>2</td>
<td>NF-κB inflammatory / survival signaling</td>
<td>NF-κB ↓; cytokines ↓ (reported)</td>
<td>Inflammatory tone modulation</td>
<td>R, G</td>
<td>Anti-inflammatory / anti-survival</td>
<td>Suppression of NF-κB contributes to reduced tumor-promoting inflammation and survival signaling.</td>
</tr>
<tr>
<td>3</td>
<td>PI3K → AKT signaling</td>
<td>PI3K/AKT ↓; proliferation ↓ (model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth signaling suppression</td>
<td>Reported in multiple cancer cell models; often secondary to upstream immune or redox modulation.</td>
</tr>
<tr>
<td>4</td>
<td>Intrinsic apoptosis (mitochondrial pathway)</td>
<td>Caspases ↑; Bax ↑; Bcl-2 ↓ (reported)</td>
<td>Minimal apoptosis in normal cells (dose-dependent)</td>
<td>G</td>
<td>Apoptotic induction</td>
<td>Apoptosis frequently reported in vitro; magnitude depends on molecular weight and sulfation.</td>
</tr>
<tr>
<td>5</td>
<td>Angiogenesis (VEGF signaling)</td>
<td>VEGF ↓; angiogenesis ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic</td>
<td>Anti-angiogenic activity is one of the more reproducible findings in preclinical systems.</td>
</tr>
<tr>
<td>6</td>
<td>Metastasis / adhesion (selectins, ECM interaction)</td>
<td>Tumor adhesion ↓; invasion ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-metastatic</td>
<td>Sulfated structure may interfere with selectin-mediated adhesion and tumor cell migration.</td>
</tr>
<tr>
<td>7</td>
<td>ROS / redox modulation</td>
<td>ROS modulation (context-dependent)</td>
<td>Antioxidant protection reported</td>
<td>P, R</td>
<td>Redox modulation (secondary)</td>
<td>Fucoidan is not a primary pro-oxidant; redox effects appear secondary to signaling changes.</td>
</tr>
<tr>
<td>8</td>
<td>Chemo / radiation synergy</td>
<td>Sensitization ↑ (reported in models)</td>
<td>↔</td>
<td>G</td>
<td>Adjunct potential</td>
<td>May enhance cytotoxic therapy response; evidence largely preclinical.</td>
</tr>
<tr>
<td>9</td>
<td>Warburg metabolism</td>
<td>Indirect modulation (not a primary glycolysis inhibitor)</td>
<td>↔</td>
<td>R</td>
<td>Metabolic secondary effect</td>
<td>Metabolic changes likely downstream of survival pathway suppression rather than direct glycolysis blockade.</td>
</tr>
<tr>
<td>10</td>
<td>Bioavailability / heterogeneity constraint</td>
<td>Effects vary by molecular weight and source</td>
<td>Generally well tolerated orally</td>
<td>—</td>
<td>Translation constraint</td>
<td>Composition varies widely by seaweed species and extraction method; standardization is critical.</td>
</tr>
</table>
<p><small>
TSF: P = 0–30 min (surface receptor interactions), R = 30 min–3 hr (immune and signaling shifts), G = >3 hr (apoptosis, angiogenesis, immune outcomes).
</small></p>