Date Fruit Extract / Fas Cancer Research Results

DFE, Date Fruit Extract: Click to Expand ⟱
Features:
Dates (the fruit of Phoenix dactylifera) have been increasingly studied for their potential anticancer and cancer-preventive properties, mainly due to their rich phytochemical content and strong antioxidant activity.
Dates contain a broad spectrum of bioactive compounds linked to cancer prevention:
-Phenolic acids – e.g., ferulic acid, gallic acid, caffeic acid, and p-coumaric acid
-Flavonoids – e.g., quercetin, luteolin, apigenin
-Carotenoids – e.g., β-carotene, lutein
-Tannins, saponins, and sterols
-Dietary fiber and polysaccharides
These compounds have antioxidant, anti-inflammatory, and antiproliferative effects.

Date fiber and polyphenols foster beneficial gut bacteria (e.g., Bifidobacterium, Lactobacillus) that produce short-chain fatty acids (SCFAs), which protect the colon and may lower colon cancer risk.

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Nrf2 / ARE antioxidant response Context-dependent modulation Nrf2 ↑; antioxidant enzymes ↑ R, G Redox buffering Polyphenol-driven antioxidant response is the dominant mechanistic theme in non-malignant systems.
2 ROS / oxidative stress modulation ROS ↓ (generally); pro-oxidant effects not dominant Oxidative stress ↓ P, R Antioxidant effect Most studies describe antioxidant protection rather than tumor-selective ROS elevation.
3 NF-κB inflammatory signaling NF-κB ↓ (reported in limited models) Inflammation tone ↓ R, G Anti-inflammatory modulation Observed in inflammatory and oxidative injury systems; tumor-specific evidence is limited.
4 Intrinsic apoptosis (mitochondrial; limited data) Apoptosis ↑ (reported in some in-vitro studies) ↔ G Conditional cytotoxicity Cytotoxic effects generally mild and concentration-dependent; not comparable to strong pro-oxidants.
5 Cell-cycle arrest Cell-cycle modulation ↑ (limited evidence) ↔ G Cytostasis (weak) Evidence exists but is inconsistent and often extract-dependent.
6 PI3K → AKT signaling Limited data; possible ↓ (reported in some systems) ↔ R, G Survival pathway modulation Not a consistently demonstrated primary mechanism.
7 Angiogenesis signaling (VEGF) Limited data; possible ↓ ↔ G Potential anti-angiogenic effect Evidence sparse compared to stronger polyphenols like gallic or caffeic acid.
8 Invasion / metastasis (MMPs) Limited evidence ↔ G Uncertain tumor relevance Not well characterized mechanistically in oncology models.
9 Metabolic modulation Indirect via anti-inflammatory and antioxidant tone Metabolic support ↑ R, G Systemic metabolic effect Better supported in cardiometabolic contexts than direct anticancer contexts.
10 Extract variability / compositional heterogeneity Activity varies by cultivar, processing, solvent — — Translation constraint Whole fruit extracts differ significantly in phenolic profile and potency.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (rapid antioxidant interactions)
  • R: 30 min–3 hr (acute transcriptional shifts)
  • G: >3 hr (gene-regulatory and phenotype-level outcomes)
Fas, Fas Death receptor: Click to Expand ⟱
Source:
Type:
Fas (also known as CD95 or APO-1) and Fas ligand (FasL) are proteins that play a crucial role in the regulation of programmed cell death, also known as apoptosis.

The Fas/FasL system is involved in the elimination of damaged or unwanted cells, including cancer cells.
Fas agonists, which mimic the action of FasL, have been shown to induce apoptosis in cancer cells. FasL inhibitors, which block the interaction between Fas and FasL, have been shown to enhance the effectiveness of chemotherapy and immunotherapy

Fas is often expressed ,and may be associated with better responses to chemotherapy, but its role in promoting cell survival in certain contexts can complicate its prognostic implications.
Scientific Papers found: Click to Expand⟱
4455- DFE,    Ajwa Date (Phoenix dactylifera L.) Extract Inhibits Human Breast Adenocarcinoma (MCF7) Cells In Vitro by Inducing Apoptosis and Cell Cycle Arrest
- in-vitro, BC, MCF-7 - in-vitro, Nor, 3T3
TumCCA↑, P53↑, BAX↑, Casp3↑, MMP↓, Fas↑, FasL↑, Bcl-2↓, Apoptosis↑, TumCP↓, TUNEL↑, eff↑, selectivity↑,

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:


Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Fas↑, 1,   FasL↑, 1,   TUNEL↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Fas, Fas Death receptor
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#:371  Target#:112  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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