Propyl gallate / Fas Cancer Research Results

PG, Propyl gallate: Click to Expand ⟱
Features:
An ester formed by the condensation of gallic acid and propanol.
Propyl gallate (PG), chemically known as propyl-3,4,5-trihydroxybenzoate, is widely present in processed food and cosmetics, hair products, and lubricants.
PG alone demonstrated antioxidative and cytoprotective properties against cellular damage and gained a pro-oxidative property in combination with copper (II). It was reported that PG was one of the most active compounds capable of generating H2O2 in DMEM media
Main cancer-relevant pathways modulated by propyl gallate
A. Redox imbalance & oxidative stress (dominant)
-↑ Intracellular ROS (context- and dose-dependent)
  -Pro-oxidant in cancer cells with high basal ROS
  -Mitochondrial superoxide accumulation
  -Thiol depletion (↓ GSH, ↓ Trx buffering capacity)
Importance: ★★★★★  (Primary mechanism)

B. Mitochondrial dysfunction & intrinsic apoptosis
-↑ MOMP → caspase cascade
  -Loss of mitochondrial membrane potential (ΔΨm)
  -Cytochrome-c release
  -Caspase-9 → caspase-3 activation
  -↑ Bax / ↓ Bcl-2 ratio
Importance: ★★★★☆

C. ER stress & unfolded protein response (UPR)
-↑ PERK–eIF2α–ATF4–CHOP
  -ROS-linked protein misfolding
  -Pro-apoptotic UPR signaling dominates over adaptive UPR
Importance: ★★★☆☆

D. Cell cycle disruption
-G1 or G2/M arrest (cell-type dependent)
  -↓ Cyclin D1, Cyclin B1
  -↑ p21, p27
Importance: ★★☆☆☆

E. MAPK stress signaling
-↑ JNK / p38
  -Stress-activated apoptosis signaling
  -Often precedes mitochondrial failure
Importance: ★★☆☆☆

F. Inflammation & survival pathways (secondary)
-↓ NF-κB, ↓ STAT3 (indirect)
  -Suppression is largely ROS-mediated, not direct inhibition
  -Reduced anti-apoptotic gene transcription
Importance: ★★☆☆☆

G. NRF2–ARE signaling (dual role)
-Low dose: NRF2 activation → cytoprotection
  -High dose / cancer cells: NRF2 overwhelmed → apoptosis
Importance: ★★☆☆☆
(Highly context dependent; double-edged)
Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 Glutathione (GSH) redox buffering ↓ GSH (depletion) Upstream redox vulnerability Leukemia and HeLa models report GSH depletion as an early, causal event in PG-induced cytotoxicity (ref)
2 Nrf2 antioxidant-response axis ↓ Nrf2 nuclear translocation → ↓ γ-GCS Impaired antioxidant capacity PG inhibits Nrf2 nuclear translocation and downstream glutathione-synthesis control, linking to GSH depletion and apoptosis in leukemia cells (ref)
3 Reactive oxygen species (ROS) balance (context-dependent) ↑ ROS (tumor models) / ↓ ROS (TMZ-combo migration model) Oxidative-stress modulation PG increases ROS in hepatocellular carcinoma (HCC) with autophagy/apoptosis; in TMZ-treated glioma, PG inhibits TMZ-induced ROS linked to reduced migration (ref)
4 MAPK stress signaling (ERK/JNK/p38) ↑ MAPK activation Stress-to-death signaling PG activates MAPKs; authors position MAPKs/Nrf2-mediated GSH depletion as an early driver of apoptosis (ref)
5 Autophagy program (LC3 conversion) ↑ autophagy Stress response contributing to growth inhibition HCC study: PG induces ROS and activates autophagy (LC3-I→LC3-II), with associated apoptosis markers (ref)
6 Apoptosis (caspase cascade; intrinsic/extrinsic components) ↑ caspase activation / ↑ apoptosis Programmed cell death Leukemia: caspases-3/8/9 activation with p53/Bax/Fas/FasL changes; lung cancer: caspase-dependent apoptosis with PARP cleavage (ref)
7 Cell-cycle regulation ↑ G1 arrest (e.g., ↑ p27) Proliferation blockade HeLa and lung cancer models report PG-induced G1 phase arrest with cell-cycle regulator changes (ref)
8 Lung cancer growth suppression ↓ proliferation / ↓ viability Anti-growth effect PG reduces growth of Calu-6 and A549 lung cancer cells with G1 arrest and caspase-dependent apoptosis (ref)
9 Migration / invasion phenotype (TMZ-combination glioma model) ↓ migration (via ↓ TMZ-induced ROS; NF-κB pathway implicated in full paper title) Anti-migratory effect (combination context) TMZ + PG enhances inhibition of U87MG glioma migration; abstract states PG inhibits TMZ-induced ROS and implicates mitochondrial complex III / NADPH oxidase as ROS sources (ref)
10 In vivo anti-tumor effect (HCC; zebrafish model) ↓ tumor growth / ↓ proliferation Demonstrated in vivo activity HCC study includes in vivo suppression (zebrafish) alongside ROS increase and autophagy activation (ref)


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⟱
5217- PG,    Role of redox signaling regulation in propyl gallate-induced apoptosis of human leukemia cells
- in-vitro, AML, THP1 - in-vitro, AML, Jurkat - in-vitro, AML, HL-60
tumCV↓, Casp3↑, Casp8↑, Casp9↑, P53↑, BAX↑, Fas↑, FasL↑, MAPK↑, NRF2↓, GSH↓,

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:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   NRF2↓, 1,  

Cell Death ⓘ

BAX↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Fas↑, 1,   FasL↑, 1,   MAPK↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  
Total Targets: 11

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#:138  Target#:112  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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