Pterostilbene / cMyc Cancer Research Results

PTS, Pterostilbene: Click to Expand ⟱
Features:
Antioxidant found in blueberries, cranberries and grapes.
Pterostilbene (trans-3,5-dimethoxy-40-hydroxystilbene) is a naturally occurring stilbene, found mainly in blueberries and grapes. It is a dimethylated derivative of resveratrol with comparable antioxidant, anti-inflammatory and anticarcinogenic properties [26].
-more bioavailable than resveratrol
-Antioxidant activity: Reduces reactive oxygen species and lipid peroxidation
-Anti-inflammatory: Downregulates pro-inflammatory cytokines- IL-1β, TNF-α, NF-κB
-Amyloid pathology:inhibits Aβ aggregation and promotes clearance- Aβ, APP, BACE1
-Reduces hyperphosphorylation of tau protein
-Inhibits histone deacetylases (HDACs)
-Increases acetylcholine by inhibiting acetylcholinesterase
-Sirtuin activation

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 SIRT1 / AMPK metabolic sensing ↑ AMPK; context-dependent SIRT1 modulation ↑ SIRT1 / ↑ AMPK Driver Energy-stress signaling Pterostilbene strongly engages energy-sensing pathways due to high bioavailability
2 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Driver Growth and survival inhibition AKT/mTOR suppression explains cytostatic and pro-apoptotic effects in cancer cells
3 Reactive oxygen species (ROS) ↑ ROS (mild, dose-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation More balanced redox profile than resveratrol; weaker pro-oxidant behavior
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Secondary Execution of apoptosis Mitochondrial apoptosis follows metabolic and redox stress
5 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of inflammatory survival programs NF-κB inhibition contributes to anti-invasive and chemosensitizing effects
6 Cell cycle regulation ↑ G1 or G2/M arrest ↔ spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream metabolic and signaling effects
7 NRF2 antioxidant response ↑ NRF2 (adaptive) ↑ NRF2 (protective) Adaptive Redox compensation NRF2 activation contributes to stress buffering rather than primary cytotoxicity


cMyc, cellular-MYC oncogene: Click to Expand ⟱
Source:
Type: oncogene
The MYC proto-oncogenes are among the most commonly activated proteins in human cancer. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. The c-Myc oncogene is a ‘master regulator’ of both cellular growth and metabolism in transformed cells.
-C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A

Inhibitors (downregulate):
Curcumin
Resveratrol: downregulate c-Myc expression.
Epigallocatechin Gallate (EGCG)
Quercetin
Berberine: decrease c-Myc expression and repress its transcriptional activity.
Scientific Papers found: Click to Expand⟱
4694- PTS,    Pterostilbene as a Multifaceted Anticancer Agent: Molecular Mechanisms, Therapeutic Potential and Future Directions
BioAv↑, AntiCan↑, Casp↑, TumCCA↑, angioG↓, TumMeta↓, MMP9↓, VEGF↓, CSCs↓, CD44↓, cMyc↓, ChemoSen↑, mTOR↓,
2408- PTS,    Pterostilbene suppresses the growth of esophageal squamous cell carcinoma by inhibiting glycolysis and PKM2/STAT3/c-MYC signaling pathway
- in-vitro, ESCC, NA
TumCP↓, TumCMig↓, PKA↓, GlucoseCon↓, lactateProd↓, PKM2↓, STAT3↓, cMyc↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis ⓘ

cMyc↓, 2,   GlucoseCon↓, 1,   lactateProd↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Casp↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   mTOR↓, 1,   STAT3↓, 1,  

Migration ⓘ

MMP9↓, 1,   PKA↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene
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#:139  Target#:35  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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