Pterostilbene / TumCI 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


TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
4699- PTS,    Pterostilbene inhibits triple-negative breast cancer metastasis via inducing microRNA-205 expression and negatively modulates epithelial-to-mesenchymal transition
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, HS587T - in-vivo, BC, MDA-MB-231
TumCMig↓, TumCI↓, E-cadherin↑, Snail↓, Slug↓, Vim↓, Zeb1↑, miR-205↑, Src↓, TumCG↓, FAK↓, EMT↓,
4689- PTS,    Pterostilbene Suppresses both Cancer Cells and Cancer Stem-Like Cells in Cervical Cancer with Superior Bioavailability to Resveratrol
eff↑, TumCCA↑, ROS↑, MMP2↓, MMP9↓, CSCs↓, CD133↓, OCT4↓, SOX2↓, Nanog↓, STAT3↓, BioAv↑, TumCI↓, ROS↑, Apoptosis↑,
1237- PTS,    Pterostilbene induces cell apoptosis and inhibits lipogenesis in SKOV3 ovarian cancer cells by activation of AMPK-induced inhibition of Akt/mTOR signaling cascade
- in-vitro, Ovarian, SKOV3
TumCMig↓, TumCI↓, MDA↑, ROS↑, BAX↑, Casp3↑, Bcl-2↓, SREBP1↓, FASN↓, AMPK↓, p‑AMPK↑, p‑P53↑, p‑TSC2↑, p‑Akt↓, p‑mTOR↓, p‑S6K↓, p‑4E-BP1↓,
1238- PTS,    Pterostilbene suppresses gastric cancer proliferation and metastasis by inhibiting oncogenic JAK2/STAT3 signaling: In vitro and in vivo therapeutic intervention
- in-vitro, GC, NA - in-vivo, NA, NA
TumCCA↑, TumCP↓, TumCMig↓, TumCI↓, TumVol↓, TumW↓, Weight∅, JAK2↓, STAT3↓,
3929- PTS,    New Insights into Dietary Pterostilbene: Sources, Metabolism, and Health Promotion Effects
- Review, Var, NA - Review, Arthritis, NA
*NRF2↑, *BioAv↑, *ROS↓, *Inflam↓, *HO-1↑, *SOD↑, *Catalase↑, *GPx↑, *lipid-P↓, *hepatoP↑, *neuroP↑, *iNOS↓, *COX2↓, TumMeta↓, SOD2↓, ROS↑, TumCI↓, TumCG↓, HDAC1↓, PTEN↑, BP↓, *GutMicro↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

MDA↑, 1,   ROS↑, 4,   SOD2↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   p‑AMPK↑, 1,   FASN↓, 1,   p‑S6K↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,  

Kinase & Signal Transduction ⓘ

p‑TSC2↑, 1,  

Transcription & Epigenetics ⓘ

miR-205↑, 1,  

DNA Damage & Repair ⓘ

p‑P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   CD133↓, 1,   CSCs↓, 1,   EMT↓, 1,   HDAC1↓, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PTEN↑, 1,   SOX2↓, 1,   Src↓, 1,   STAT3↓, 2,   TumCG↓, 2,  

Migration ⓘ

E-cadherin↑, 1,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   Slug↓, 1,   Snail↓, 1,   TumCI↓, 5,   TumCMig↓, 3,   TumCP↓, 1,   TumMeta↓, 1,   Vim↓, 1,   Zeb1↑, 1,  

Immune & Inflammatory Signaling ⓘ

JAK2↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,   TumW↓, 1,   Weight∅, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 14

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
5 Pterostilbene
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#:324  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page