Moringa oleifera / GSTs Cancer Research Results

Moringa, Moringa oleifera: Click to Expand ⟱
Features:
The leaves, seeds, and pods of the Moringa oleifera plant 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.
Moringa oleifera extracts on various types of cancer: Breast, Lung, Colon, Prostate
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

  • P: 0–30 min (rapid redox interactions)
  • R: 30 min–3 hr (acute signaling shifts)
  • G: >3 hr (gene-regulatory and phenotype-level outcomes)

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).
GSTs, Glutathione S-transferases: Click to Expand ⟱
Source:
Type:
Glutathione S-transferases (GSTs) are a family of phase II detoxification enzymes that play key roles in catalyzing the conjugation of glutathione (GSH) to a wide range of electrophilic compounds. This family includes multiple isoenzymes (e.g., GST-α, GST-μ, GST-π) with tissue-specific expression patterns and overlapping as well as distinct substrate specificities.

-GSTs are important for detoxifying potentially harmful compounds, including products of oxidative stress, environmental toxins, and chemotherapeutic agents.
-They contribute to the cellular defense mechanism against oxidative damage and help maintain cellular redox balance.
-Beyond detoxification, GSTs can modulate cell signaling pathways, potentially affecting cell proliferation, apoptosis, and drug resistance.

-GST-π is commonly upregulated in several cancers such as breast, lung, colorectal, and hematologic malignancies.
-Elevated expression of specific GST isoenzymes—most notably GST-π—has been associated with a poorer prognosis in several cancer types. This is often linked to resistance to chemo- or radiotherapy, as higher GST activity can lead to more efficient detoxification of these agents, reducing their cytotoxic effects.
-In contrast, reduced GST expression in some contexts might indicate a less robust detoxification system, which can correlate with increased sensitivity to oxidative stress and possibly a less aggressive tumor phenotype.
Scientific Papers found: Click to Expand⟱
3844- Moringa,    Review of the Safety and Efficacy of Moringa oleifera
- Review, NA, NA
*antiOx↑, *RenoP↑, *hepatoP↑, *radioP↑, *eff↑, *toxicity↓, *ROS↓, *lipid-P↓, *DNAdam↓, *Catalase↑, *SOD↑, *GPx↑, *GSR↑, *GSTs↑, *AST↓, *ALAT↓, *ALP↓, *Bil↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Bil↓, 1,   Catalase↑, 1,   GPx↑, 1,   GSR↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   Bil↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 20

Scientific Paper Hit Count for: GSTs, Glutathione S-transferases
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:209  Target#:1153  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

Home Page