Pterostilbene / JNK 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


JNK, c-Jun N-terminal kinase (JNK): Click to Expand ⟱
Source:
Type:
JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. Janus signaling promotes cancer cell survival.
JNK, or c-Jun N-terminal kinase, is a member of the mitogen-activated protein kinase (MAPK) family. It plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). JNK is activated in response to various stress signals, such as UV radiation, oxidative stress, and inflammatory cytokines.
JNK activation can promote apoptosis in cancer cells, acting as a tumor suppressor. However, in other contexts, it can promote cell survival and proliferation, contributing to tumor progression.

JNK is often unregulated in cancers, leading to increased cancer cell proliferation, survival, and resistance to apoptosis. This activation is typically associated with poor prognosis and aggressive tumor behavior.
Scientific Papers found: Click to Expand⟱
3919- PTS,    Low-dose pterostilbene, but not resveratrol, is a potent neuromodulator in aging and Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, *SIRT1∅, *PPARα↑, *SOD2↑, *JNK↓, *p‑tau↓,

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 ⓘ

SOD2↑, 1,  

Core Metabolism/Glycolysis ⓘ

PPARα↑, 1,   SIRT1∅, 1,  

Cell Death ⓘ

JNK↓, 1,  

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: JNK, c-Jun N-terminal kinase (JNK)
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#:168  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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