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.
| Rank | Pathway / Axis | Cancer / Tumor Context | Normal Tissue Context | TSF | Primary Effect | Notes / Interpretation |
|---|---|---|---|---|---|---|
| 1 | NF-κB inflammatory signaling | NF-κB ↓; COX-2, IL-6, TNF-α ↓ (reported) | Inflammation tone ↓ | R, G | Anti-inflammatory / anti-survival modulation | One of the more consistently reported mechanisms across tumor and inflammatory models. |
| 2 | ROS / Redox modulation (context-dependent) | ROS ↑ in some tumor models (extract-dependent) | ROS ↓; antioxidant protection | P, R | Biphasic redox modulation | Leaf extracts often antioxidant; certain fractions (isothiocyanates) may elevate ROS in tumor cells. |
| 3 | Nrf2 / ARE pathway | Context-dependent modulation | Nrf2 ↑; antioxidant enzymes ↑ | R, G | Redox buffering | Common polyphenol/isothiocyanate signature; tumor impact varies and may influence therapy sensitivity. |
| 4 | PI3K → AKT (± mTOR) | PI3K/AKT ↓ (reported; model-dependent) | ↔ | R, G | Growth/survival suppression | Frequently secondary to inflammatory and oxidative stress pathway changes. |
| 5 | MAPK pathways (ERK / JNK / p38) | Stress MAPK modulation (JNK/p38 ↑ reported) | ↔ | P, R, G | Signal reprogramming | Often associated with ROS-mediated apoptosis in tumor cells. |
| 6 | Intrinsic apoptosis (mitochondrial) | ΔΨm ↓; Bax ↑; caspases ↑ (reported) | ↔ (limited activation) | G | Cell death execution | Observed in several cancer cell lines; magnitude depends on extract concentration and composition. |
| 7 | Cell-cycle arrest (G1 / G2-M) | Cell-cycle arrest ↑ (reported) | ↔ | G | Cytostasis | Often associated with Cyclin/CDK modulation; phase varies by tumor model. |
| 8 | Angiogenesis signaling (VEGF) | VEGF ↓ (reported in some systems) | ↔ | G | Anti-angiogenic modulation | Evidence present but less consistent than NF-κB or redox effects. |
| 9 | Invasion / metastasis (MMPs / EMT) | MMP2/MMP9 ↓; migration ↓ (reported) | ↔ | G | Anti-invasive phenotype | Likely downstream of NF-κB and MAPK modulation. |
| 10 | Bioavailability / extract variability | Activity varies by preparation (leaf, seed, isolate) | — | — | Translation constraint | Complex phytochemistry; systemic levels from oral intake may not match in-vitro cytotoxic concentrations. |
Time-Scale Flag (TSF): P / R / G
Active fractions (context-dependent): 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).