Description: <b>Cinnamon</b> is a spice from inner bark from several tree species.<br>
Cinnamon refers primarily to bark extracts from Cinnamomum verum (Ceylon cinnamon) and Cinnamomum cassia. Bioactive constituents include cinnamaldehyde, cinnamic acid derivatives, procyanidins, and polyphenols. In cancer models, cinnamon extracts and cinnamaldehyde are most frequently reported to exert anti-proliferative, pro-apoptotic, anti-inflammatory, and anti-angiogenic effects. Mechanistic themes include suppression of NF-κB and PI3K/AKT signaling, modulation of MAPK pathways, induction of mitochondrial apoptosis, and context-dependent ROS elevation in tumor cells. Some studies report inhibition of HIF-1α and glycolytic signaling, though cinnamon is not a direct enzymatic Warburg inhibitor. Effects vary substantially depending on species (Ceylon vs Cassia), preparation (aqueous vs ethanol extract), and dose. Human oncology data remain limited and largely preclinical.
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Biological activity, cinnamaldehyde from Ceylon cinnamon:<br>
Antimicrobial activity: 10-50 μM<br>
Antioxidant activity: 10-100 μM<br>
Anti-inflammatory activity: 20-50 μM<br>
Anticancer activity: 50-100 μM<br>
Cardiovascular health: 20-50 μM<br>
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5 g of Ceylon cinnamon might contain roughly between 30 mg and 150 mg of cinnamaldehyde, with an approximate mid-range estimate of about 70 mg.<br>
Assuming a moderate supplemental intake 50–200 mg of cinnamaldehyde, peak plasma levels might be anticipated in the vicinity of 1–10 μM.<br>
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<h3>Cancer Pathway Table: Cinnamon</h3>
<!-- Cancer Pathway Table: Cinnamon -->
<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>NF-κB inflammatory / survival signaling</td>
<td>NF-κB ↓; COX-2 ↓; cytokines ↓ (reported)</td>
<td>Inflammatory tone ↓</td>
<td>R, G</td>
<td>Anti-inflammatory / anti-survival</td>
<td>One of the more consistently reported mechanisms across tumor models.</td>
</tr>
<tr>
<td>2</td>
<td>PI3K → AKT → mTOR axis</td>
<td>PI3K/AKT ↓; proliferation ↓ (model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth signaling suppression</td>
<td>Frequently observed downstream of cinnamaldehyde exposure.</td>
</tr>
<tr>
<td>3</td>
<td>Intrinsic apoptosis (mitochondrial pathway)</td>
<td>Bax ↑; Bcl-2 ↓; caspases ↑ (reported)</td>
<td>Minimal activation at lower exposure</td>
<td>G</td>
<td>Apoptotic induction</td>
<td>Apoptosis induction often associated with mitochondrial depolarization.</td>
</tr>
<tr>
<td>4</td>
<td>ROS modulation (dose-dependent)</td>
<td>ROS ↑ (tumor contexts); apoptosis ↑</td>
<td>Antioxidant activity at low exposure</td>
<td>P, R</td>
<td>Redox modulation</td>
<td>Cinnamaldehyde may increase ROS in cancer cells while acting antioxidant at lower doses.</td>
</tr>
<tr>
<td>5</td>
<td>MAPK pathways (ERK / JNK / p38)</td>
<td>Stress-MAPK modulation (context-dependent)</td>
<td>↔</td>
<td>P, R, G</td>
<td>Signal reprogramming</td>
<td>JNK/p38 activation reported in apoptosis models; ERK modulation varies.</td>
</tr>
<tr>
<td>6</td>
<td>HIF-1α / glycolysis signaling</td>
<td>HIF-1α ↓; glycolytic gene expression ↓ (reported)</td>
<td>↔</td>
<td>R, G</td>
<td>Indirect Warburg modulation</td>
<td>Not a direct enzyme inhibitor; metabolic effects appear secondary to survival pathway suppression.</td>
</tr>
<tr>
<td>7</td>
<td>Angiogenesis (VEGF signaling)</td>
<td>VEGF ↓; angiogenesis ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic</td>
<td>Observed in some in vitro and animal models.</td>
</tr>
<tr>
<td>8</td>
<td>Cell-cycle regulation (G1/G2-M arrest)</td>
<td>Cell-cycle arrest ↑ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis</td>
<td>Associated with reduced Cyclin/CDK expression.</td>
</tr>
<tr>
<td>9</td>
<td>Metastasis / EMT modulation</td>
<td>MMPs ↓; migration ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Likely downstream of NF-κB and PI3K modulation.</td>
</tr>
<tr>
<td>10</td>
<td>Safety / composition constraint (coumarin content)</td>
<td>High cassia intake may pose hepatotoxicity risk</td>
<td>Generally safe in culinary amounts</td>
<td>—</td>
<td>Translation constraint</td>
<td>Cassia cinnamon contains higher coumarin; Ceylon cinnamon preferred for higher intake.</td>
</tr>
</table>
<p><small>
TSF: P = 0–30 min (redox and early signaling effects), R = 30 min–3 hr (acute pathway modulation), G = >3 hr (apoptosis, angiogenesis, phenotype changes).
</small></p>