Description: <b>The leaves, seeds, and pods of the Moringa oleifera plant</b> contain a variety of bioactive compounds, including flavonoids, phenolic acids, and saponins, which have been shown to have anti-inflammatory, antioxidant, and anti-proliferative effects.<br>
Moringa oleifera extracts on various types of cancer: Breast, Lung, Colon, Prostate<br>
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Moringa (Moringa oleifera) is not a single compound.
Cancer-related data are primarily from:
-Leaf extracts (polyphenols, quercetin, kaempferol)
-Isothiocyanates (e.g., moringin)
-Glucosinolates
-Alkaloids and other secondary metabolites
Mechanistically it behaves as a mixed redox-modulating phytochemical extract, not a strong direct cytotoxin.
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<!-- Moringa (MOR) — Cancer-Oriented Time-Scale Flagged Pathway Table -->
<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 signaling</td>
<td>NF-κB ↓; COX-2, IL-6, TNF-α ↓ (reported)</td>
<td>Inflammation tone ↓</td>
<td>R, G</td>
<td>Anti-inflammatory / anti-survival modulation</td>
<td>One of the more consistently reported mechanisms across tumor and inflammatory models.</td>
</tr>
<tr>
<td>2</td>
<td>ROS / Redox modulation (context-dependent)</td>
<td>ROS ↑ in some tumor models (extract-dependent)</td>
<td>ROS ↓; antioxidant protection</td>
<td>P, R</td>
<td>Biphasic redox modulation</td>
<td>Leaf extracts often antioxidant; certain fractions (isothiocyanates) may elevate ROS in tumor cells.</td>
</tr>
<tr>
<td>3</td>
<td>Nrf2 / ARE pathway</td>
<td>Context-dependent modulation</td>
<td>Nrf2 ↑; antioxidant enzymes ↑</td>
<td>R, G</td>
<td>Redox buffering</td>
<td>Common polyphenol/isothiocyanate signature; tumor impact varies and may influence therapy sensitivity.</td>
</tr>
<tr>
<td>4</td>
<td>PI3K → AKT (± mTOR)</td>
<td>PI3K/AKT ↓ (reported; model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth/survival suppression</td>
<td>Frequently secondary to inflammatory and oxidative stress pathway changes.</td>
</tr>
<tr>
<td>5</td>
<td>MAPK pathways (ERK / JNK / p38)</td>
<td>Stress MAPK modulation (JNK/p38 ↑ reported)</td>
<td>↔</td>
<td>P, R, G</td>
<td>Signal reprogramming</td>
<td>Often associated with ROS-mediated apoptosis in tumor cells.</td>
</tr>
<tr>
<td>6</td>
<td>Intrinsic apoptosis (mitochondrial)</td>
<td>ΔΨm ↓; Bax ↑; caspases ↑ (reported)</td>
<td>↔ (limited activation)</td>
<td>G</td>
<td>Cell death execution</td>
<td>Observed in several cancer cell lines; magnitude depends on extract concentration and composition.</td>
</tr>
<tr>
<td>7</td>
<td>Cell-cycle arrest (G1 / G2-M)</td>
<td>Cell-cycle arrest ↑ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis</td>
<td>Often associated with Cyclin/CDK modulation; phase varies by tumor model.</td>
</tr>
<tr>
<td>8</td>
<td>Angiogenesis signaling (VEGF)</td>
<td>VEGF ↓ (reported in some systems)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic modulation</td>
<td>Evidence present but less consistent than NF-κB or redox effects.</td>
</tr>
<tr>
<td>9</td>
<td>Invasion / metastasis (MMPs / EMT)</td>
<td>MMP2/MMP9 ↓; migration ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Likely downstream of NF-κB and MAPK modulation.</td>
</tr>
<tr>
<td>10</td>
<td>Bioavailability / extract variability</td>
<td>Activity varies by preparation (leaf, seed, isolate)</td>
<td>—</td>
<td>—</td>
<td>Translation constraint</td>
<td>Complex phytochemistry; systemic levels from oral intake may not match in-vitro cytotoxic concentrations.</td>
</tr>
</table>
<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (rapid redox interactions)</li>
<li><b>R</b>: 30 min–3 hr (acute signaling shifts)</li>
<li><b>G</b>: >3 hr (gene-regulatory and phenotype-level outcomes)</li>
</ul>
<p><b>Active fractions (context-dependent):</b> Leaf polyphenols (quercetin/kaempferol-class), glucosinolates/isothiocyanates (moringin-class), and other mixed constituents. Mechanistic direction can vary by preparation (leaf vs seed; aqueous vs ethanol; standardized vs crude).</p>