Ginger/6-Shogaol/Gingerol / angioG Cancer Research Results

GI, Ginger/6-Shogaol/Gingerol: Click to Expand ⟱
Features:
Flowering plant uses ginger root for help with nausea, weight loss, arthritis, diabetes. Anti-inflammatory and antioxidant.
Gingerol is a phenolic phytochemical compound found in fresh ginger that activates heat receptors on the tongue. It is normally found as a pungent yellow oil in the ginger rhizome.
Ginger contains multiple bioactive compounds including 6-gingerol, 8-gingerol, 10-gingerol, 6-shogaol, paradols, and zingerone.
In cancer-focused literature, the majority of mechanistic work centers on 6-gingerol and 6-shogaol.
Mechanistic themes (preclinical):
-Anti-inflammatory (NF-κB↓, COX-2↓)
-Survival pathway modulation (PI3K/AKT↓, STAT3↓ reported)
-MAPK modulation (ERK/JNK/p38 context-dependent)
-ROS modulation (antioxidant in normal cells; pro-oxidant at higher doses in tumor models)
-Cell-cycle arrest (G1 or G2/M reported)
-Apoptosis induction (mitochondrial pathway)
-Anti-angiogenic and anti-metastatic signaling (VEGF↓, MMPs↓ reported)

Bioavailability note:
-Gingerols are rapidly metabolized (glucuronidation/sulfation)
-Plasma levels after dietary intake are far below many in-vitro micromolar doses
-6-Shogaol is generally more potent than 6-gingerol in cell systems

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 NF-κB inflammatory transcription NF-κB ↓; COX-2 ↓; pro-inflammatory cytokines ↓ (reported) Inflammation tone ↓ R, G Anti-inflammatory / anti-survival transcription One of the most consistent ginger signatures; reduction of inflammatory tumor-support signaling.
2 PI3K → AKT (± mTOR) survival axis PI3K/AKT ↓ (reported; model-dependent) ↔ R, G Growth/survival modulation Often described in conjunction with apoptosis and proliferation reduction.
3 ROS / redox modulation (biphasic) ROS ↑ (at higher doses); apoptosis ↑ ROS ↓; antioxidant activity P, R Redox destabilization (tumor) / buffering (normal) Gingerols and shogaols may act antioxidant in normal tissue but pro-oxidant in tumor systems under higher concentrations.
4 Intrinsic apoptosis (mitochondrial pathway) ΔΨm ↓; Bax ↑; caspase-3 ↑ (reported) ↔ (less activation) G Apoptosis execution Often downstream of ROS and survival-pathway suppression.
5 Cell-cycle arrest (G1 or G2/M) Cell-cycle arrest ↑ (reported) ↔ G Cytostasis Associated with modulation of Cyclins/CDKs; phase varies by tumor type.
6 MAPK pathways (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming JNK/p38 activation often linked to stress-induced apoptosis; ERK direction varies.
7 STAT3 signaling STAT3 ↓ (reported) ↔ R, G Transcriptional survival suppression Observed in certain tumor models; contributes to reduced proliferation and invasion.
8 Angiogenesis signaling (VEGF) VEGF ↓ (reported) ↔ G Anti-angiogenic support Typically a downstream effect of inflammatory and survival pathway suppression.
9 Invasion / metastasis (MMPs / EMT) MMP-2/MMP-9 ↓; migration ↓ (reported) ↔ G Anti-invasive phenotype Frequently linked to NF-κB and STAT3 suppression.
10 Bioavailability constraint Systemic free gingerol levels low; rapid conjugation — — Translation constraint In-vitro cytotoxic concentrations often exceed achievable plasma levels after dietary intake.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (early redox and kinase interactions)
  • R: 30 min–3 hr (acute signaling shifts: NF-κB, PI3K/AKT, MAPK)
  • G: >3 hr (gene-regulatory adaptation, apoptosis, phenotype outcomes)
angioG, angiogenesis: Click to Expand ⟱
Source:
Type:
Process through which new blood vessels.
Angiogenesis, the process of new blood vessel formation from pre-existing vessels, plays a crucial role in cancer progression and metastasis. Tumors require a blood supply to grow beyond a certain size and to spread to other parts of the body.
Vascular Endothelial Growth Factor (VEGF): VEGF is one of the most important pro-angiogenic factors. It stimulates endothelial cell proliferation and migration, leading to the formation of new blood vessels. Many tumors overexpress VEGF, which correlates with poor prognosis.
Hypoxia-Inducible Factor (HIF): In response to low oxygen levels (hypoxia), tumors can activate HIF, which in turn promotes the expression of VEGF and other angiogenic factors. This mechanism allows tumors to adapt to their microenvironment and sustain growth.
Scientific Papers found: Click to Expand⟱
1005- GI,    Ginger Constituent 6-Shogaol Inhibits Inflammation- and Angiogenesis-Related Cell Functions in Primary Human Endothelial Cells
- vitro+vivo, Nor, HUVECs
*NF-kB↓, *p65↓, *TLR4∅, *angioG↓, *TumCP↓, *VEGF↓, *Inflam↓, *ICAM-1↓, *VCAM-1↓, *E-sel↓, *p‑JNK↓, *HO-1↑,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,  

Cell Death ⓘ

p‑JNK↓, 1,  

Migration ⓘ

E-sel↓, 1,   TumCP↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

ICAM-1↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   p65↓, 1,   TLR4∅, 1,  
Total Targets: 12

Scientific Paper Hit Count for: angioG, angiogenesis
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#:88  Target#:447  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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