Pterostilbene / Cyt‑c 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


Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.


Scientific Papers found: Click to Expand⟱
3930- PTS,    A Review of Pterostilbene Antioxidant Activity and Disease Modification
- Review, Var, NA - Review, adrenal, NA - Review, Stroke, NA
*BioAv↑, *antiOx↑, *neuroP↑, *Inflam↓, *ROS↓, *H2O2↓, *GSH↑, *GPx↑, *GSR↑, *SOD↑, TumCG↓, PTEN↑, HGF/c-Met↓, PI3K↓, Akt↓, NF-kB↓, TumMeta↓, MMP2↓, MMP9↓, Ki-67↓, Casp3↑, MMP↓, H2O2↑, ROS↑, ChemoSen↑, *cardioP↑, *CDK2↓, *CDK4↓, *cycE/CCNE↓, *cycD1/CCND1↓, *RB1↓, *PCNA↓, *CREB↑, *GABA↑, *memory↑, *IGF-1↑, *ERK↑, TIMP1↑, BAX↑, Cyt‑c↑, Diablo↑, SOD2↑,

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

H2O2↑, 1,   ROS↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 1,  

Cell Death

Akt↓, 1,   BAX↑, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   HGF/c-Met↓, 1,  

Proliferation, Differentiation & Cell State

PI3K↓, 1,   PTEN↑, 1,   TumCG↓, 1,  

Migration

Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TIMP1↑, 1,   TumMeta↓, 1,  

Immune & Inflammatory Signaling

NF-kB↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,  

Clinical Biomarkers

Ki-67↓, 1,  
Total Targets: 21

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   GPx↑, 1,   GSH↑, 1,   GSR↑, 1,   H2O2↓, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis

CREB↑, 1,  

DNA Damage & Repair

PCNA↓, 1,  

Cell Cycle & Senescence

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   RB1↓, 1,  

Proliferation, Differentiation & Cell State

ERK↑, 1,   IGF-1↑, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,  

Synaptic & Neurotransmission

GABA↑, 1,  

Drug Metabolism & Resistance

BioAv↑, 1,  

Functional Outcomes

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
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#:77  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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