| 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 |