Moringa oleifera / ACE/ACE1 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).
ACE/ACE1, Angiotensin-Converting Enzyme 1: Click to Expand ⟱
Source:
Type:

ACE - Angiotensin-Converting Enzyme 1

Abbreviation: ACE, ACE1, CD143

Type: Zinc metallopeptidase / renin-angiotensin system enzyme

Function: Converts angiotensin I to the biologically active vasoconstrictor angiotensin II and degrades bradykinin. ACE regulates blood pressure, vascular function, inflammation, oxidative stress, fibrosis, angiogenesis, and tissue remodeling through the classical renin-angiotensin system.

Cancer: ↑ Increased ACE/angiotensin II signaling can promote tumor-associated inflammation, angiogenesis, proliferation, fibrosis, invasion, and metastasis, particularly through downstream AT1R signaling. ACE inhibition can suppress tumor growth and angiogenic signaling in several experimental cancer models.

Alzheimer's Disease: ↕ Context-dependent. ACE participates in potentially harmful angiotensin II-mediated vascular, oxidative, and inflammatory signaling, but also directly degrades amyloid-β and can convert Aβ42 toward Aβ40. ACE levels and activity therefore show complex compartment-dependent relationships with Alzheimer's pathology.
Scientific Papers found: Click to Expand⟱
7367- HibSad,  CUR,  Moringa,  CAP,  RosA  Natural angiotensin converting enzyme inhibitors: A safeguard against hypertension, respiratory distress syndrome, and chronic kidney diseases
- Review, Nor, NA
*ACE/ACE1↓,

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:


NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: ACE/ACE1, Angiotensin-Converting Enzyme 1
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#:1629  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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