| Rank |
Pathway / Axis |
Cancer Cells |
Normal Cells |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
NF-κB inflammatory / survival transcription |
NF-κB ↓; COX-2/iNOS/cytokines/Bcl-2 family/MMPs ↓ (reported) |
Inflammation tone ↓ (context) |
R, G |
Anti-inflammatory + anti-survival transcription |
One of the most frequently reported UA effects across tumor models; downstream impacts include reduced pro-survival and pro-metastatic gene programs. |
| 2 |
STAT3 axis (JAK/STAT3 signaling) |
STAT3 activity ↓ (reported); downstream targets ↓ |
↔ |
R, G |
Oncogenic transcription suppression |
UA is often reported to suppress STAT3 signaling, contributing to reduced proliferation/survival signaling. |
| 3 |
PI3K → AKT (± mTOR) survival axis |
PI3K/AKT ↓; mTORC1 tone ↓ (reported; model-dependent) |
↔ |
R, G |
Growth/survival modulation |
Commonly listed mechanism; direction and strength vary by cell line and exposure. |
| 4 |
MAPK re-wiring (ERK / JNK / p38) |
Stress-MAPK modulation (context-dependent) |
↔ |
P, R, G |
Signal reprogramming |
JNK/p38 activation and ERK modulation are reported variably; avoid fixed arrows unless tied to a specific model. |
| 5 |
Cell-cycle checkpoints (Cyclins/CDKs; p21/p27) |
Cell-cycle arrest ↑ (G1/S or G2/M; reported); Cyclin D1/CDKs ↓ (context) |
↔ |
G |
Cytostasis |
Often downstream of NF-κB/STAT3/PI3K signaling suppression. |
| 6 |
Intrinsic apoptosis (mitochondrial/caspase linked) |
Apoptosis ↑; Bax ↑; Bcl-2 ↓; caspases ↑ (reported) |
↔ (generally less activation) |
G |
Cell death execution |
Common downstream endpoint; can be coupled to stress signaling and survival pathway suppression. |
| 7 |
Angiogenesis signaling (VEGF / HIF-1α outputs) |
VEGF ↓; angiogenic outputs ↓ (reported) |
↔ |
G |
Anti-angiogenic support |
Typically phenotype-level effects tied to NF-κB/PI3K/HIF programs. |
| 8 |
Invasion / metastasis programs (MMPs / EMT) |
MMP2/MMP9 ↓; EMT markers ↓; migration/invasion ↓ (reported) |
↔ |
G |
Anti-invasive phenotype |
Often downstream of NF-κB/STAT3 changes; not universal across all tumors. |
| 9 |
ROS / redox modulation |
ROS direction variable; redox stress or buffering reported (context) |
Oxidative injury ↓ in some non-tumor stress models |
P, R, G |
Stress modulation |
UA is not a reliable “pro-oxidant killer”; redox effects depend on dose, model, and baseline oxidative state. |
| 10 |
Bioavailability / formulation constraint |
Systemic exposure often limited (poor solubility) |
— |
— |
Translation constraint |
UA is highly lipophilic with poor aqueous solubility; many formulations (e.g., nanoparticles, phospholipid complexes) are explored to improve exposure. |