| Rank |
Pathway / Axis |
Cancer Cells |
Normal Cells |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
NF-κB inflammatory transcription |
NF-κB ↓; cytokines/COX-2/iNOS programs ↓ (reported) |
Inflammation tone ↓ (common in injury models) |
R, G |
Anti-inflammatory / anti-survival transcription |
CA is frequently reported to reduce NF-κB signaling in inflammatory and cancer models. Note: CAPE (the ester) is the “stronger” canonical NF-κB inhibitor; keep CA claims qualified as “reported.” |
| 2 |
Nrf2/ARE antioxidant response (HO-1, GSH systems) |
Stress adaptation modulation (context-dependent) |
Nrf2 ↑; HO-1 ↑; antioxidant defenses ↑ |
R, G |
Endogenous antioxidant upshift |
CA can activate Nrf2/ARE programs in oxidative stress settings; tumor direction is model-dependent and should not be overstated as uniformly “good” or “bad.” |
| 3 |
ROS / redox tone (antioxidant vs Cu-linked pro-oxidant) |
ROS direction variable; pro-oxidant DNA damage reported with Cu (context) |
Oxidative injury ↓ in many stress models |
P, R, G |
Redox modulation |
CA is classically antioxidant, yet Cu-mediated pro-oxidant DNA breakage has been described in vitro; treat as conditional (metal availability, dose, cell type). |
| 4 |
Intrinsic apoptosis (mitochondrial/caspase linked) |
Apoptosis ↑; Bax ↑; caspases ↑ (reported) |
↔ (generally less activation) |
G |
Cell death execution |
Frequently observed downstream endpoint in tumor models, often coupled to NF-κB/PI3K/MAPK and stress/redox changes. |
| 5 |
Cell-cycle control (Cyclins/CDKs; checkpoints) |
Cell-cycle arrest ↑ (reported; phase varies) |
↔ |
G |
Cytostasis |
Often appears as later phenotype-level outcome after upstream signaling shifts. |
| 6 |
PI3K → AKT (± mTOR) survival axis |
PI3K/AKT ↓ (reported; model-dependent) |
↔ |
R, G |
Growth/survival modulation |
Reported in multiple tumor systems; best kept as “reported/model-dependent,” not a primary direct target. |
| 7 |
MAPK re-wiring (ERK / JNK / p38) |
MAPK modulation (context-dependent) |
↔ |
P, R, G |
Stress/mitogenic signaling adjustment |
Directions vary across models and doses; avoid fixed arrows without a specific cited study for your cancer type. |
| 8 |
Invasion / metastasis programs (MMPs / EMT) |
MMPs ↓; migration/invasion ↓ (reported) |
↔ |
G |
Anti-invasive phenotype |
Often downstream of NF-κB/MAPK and inflammation changes; not universal across all cell lines. |
| 9 |
Angiogenesis signaling (VEGF & related outputs) |
VEGF / angiogenic outputs ↓ (reported) |
↔ |
G |
Anti-angiogenic support |
Later phenotype-level outcome; strength depends on model and exposure. |
| 10 |
Bioavailability / metabolism constraint (chlorogenic acids → conjugates) |
Systemic exposure mostly as glucuronide/sulfate/methylated metabolites |
— |
— |
Translation constraint |
After oral intake, CA/chlorogenic acids appear predominantly as conjugated metabolites; free CA levels are typically far below many in-vitro (µM) assay doses. |