Garcinol / NF-kB Cancer Research Results

GAR, Garcinol: Click to Expand ⟱
Features:
Found in dried fruit rind of Garcinia Indica with anti-inflammatory, antioxidant, anticancer, and antibacterial properties
Garcinia Cambogia Extract.
"We conclude that patients who are T-cadherin-positive could especially benefit from a therapy with garcinol."

🔬1) NF-κB & AP-1 Suppression
Garcinol inhibits NF-κB and AP-1 transcriptional activity in multiple cancer cell systems, reducing pro-inflammatory and pro-survival gene expression.
📚 2) Epigenetic Regulation
Garcinol is one of the few natural products shown to inhibit p300/CBP histone acetyltransferases, shifting chromatin acetylation and influencing gene expression (differentiation, apoptosis, EMT). This is more specific than general “HDAC modulation.”
💀 3) Apoptosis
Studies report modulation of the Bcl-2 family and increased caspase activity, but this is often downstream of transcription/epigenetic changes, not a direct redox trigger.
🧬 4) Cell Cycle & Proliferation
Lower Cyclin D1, higher p21/p27, and G1/S arrest are common phenotypes.
🧭 5) Invasion & Angiogenesis
Garcinol reduces MMP-2/9 and angiogenic markers in multiple tumor cell assays.

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB / AP-1 signaling NF-κB ↓; AP-1 ↓; downstream pro-survival/inflammatory outputs ↓ ↔ or anti-inflammatory modulation in immune cells R, G Pro-survival & inflammatory transcription suppression Garcinol is reported to inhibit NF-κB and AP-1 transcriptional activity, reducing inflammation and pro-growth signaling in multiple models.
2 Epigenetic regulation (HAT/HDAC modulation) Inhibition of p300/CBP histone acetyltransferase; altered acetylation patterns ↔ baseline epigenetic state R, G Gene regulatory reprogramming Garcinol directly inhibits histone acetyltransferases (especially p300/CBP), influencing chromatin state and gene expression linked to differentiation and proliferation.
3 Intrinsic apoptosis (mitochondrial / caspase-linked) ↑ Bax/Bak; ↓ Bcl-2/Bcl-xL; ↑ caspase-9/3 ↔ minimal activation in normal cells G Execution of apoptosis Often downstream of stress and survival pathway modulation; not as dominant as classic pro-oxidant molecules but consistent in many cell lines.
4 Cell-cycle checkpoints (p21/p27; Cyclin D1) Cell-cycle arrest (often G1/S); Cyclin D1 ↓ ↔ G Cytostasis Frequently reported as later phenotypic outcome tied to reduced proliferation.
5 Invasion / metastasis programs (MMPs / EMT) MMP-2/9 ↓; invasion/migration ↓; EMT markers ↓ ↔ G Anti-invasive phenotype Linked mechanistically to NF-κB/AP-1 and epigenetic changes influencing MMP expression and EMT regulators.
6 Angiogenesis signaling (VEGF & pro-angiogenic factors) VEGF ↓; pro-angiogenic markers ↓ ↔ G Anti-angiogenic support Sometimes measured in later in vivo or emulated assay systems; reflects downstream gene expression changes.
7 PI3K/AKT / survival kinases ↓ PI3K/AKT signaling (model-dependent) ↔ R, G Survival/growth suppression Modulation of survival kinases is reported in some systems but not a universal primary mechanism.
8 ROS / oxidative stress (context–dependent) ROS modulation (inconsistent across models) ↔ P, R, G Conditional stress modulation Some studies report mild ROS changes, but garcinol is not a strong pro-oxidant driver like BetA or curcumin in cancer cells.
9 Chemo-sensitization / combination relevance Enhanced sensitivity to chemotherapeutics (context) — G Combination leverage Combination effects are reported in selected cell lines/model systems; not universal.
10 Bioavailability constraint (oral exposure / formulation dependence) Systemic exposure often limited without enhanced delivery — — Translation constraint Poor native bioavailability is common across polyphenols/bzp molecules; formulations improve systemic exposure.

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

  • P: 0–30 min (primary/physical-chemical effects; rapid signaling / kinase shifts)
  • R: 30 min–3 hr (acute stress-response and transcription signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
822- GAR,    Garcinol, a Polyisoprenylated Benzophenone Modulates Multiple Proinflammatory Signaling Cascades Leading to the Suppression of Growth and Survival of Head and Neck Carcinoma
- vitro+vivo, HNSCC, NA
ROS↑, STAT3↓, cSrc↓, JAK1↓, JAK2↓, NF-kB↓, TGF-β↓, TumCG↓,
825- GAR,    Garcinol-induced apoptosis in prostate and pancreatic cancer cells is mediated by NF- kappaB signaling
- in-vitro, Pca, LNCaP - in-vitro, Pca, Bxpc-3 - in-vitro, Pca, PC3 - in-vitro, Pca, C4-2B
TumCG↓, Apoptosis↑, NF-kB↓,
828- GAR,  Cisplatin,    Garcinol Alone and in Combination With Cisplatin Affect Cellular Behavior and PI3K/AKT Protein Phosphorylation in Human Ovarian Cancer Cells
- in-vitro, Ovarian, OVCAR-3
tumCV↓, cl‑PARP↑, cl‑Casp3↑, BAX↑, p‑PI3K↓, p‑Akt↓, NF-kB↓,
798- GAR,    Garcinol, an acetyltransferase inhibitor, suppresses proliferation of breast cancer cell line MCF-7 promoted by 17β-estradiol
- in-vitro, BC, MCF-7
TumCP↓, TumCCA↑, Apoptosis↑, ac‑H3↑, ac‑H4∅, NF-kB↓, ac‑p65↑, cycD1/CCND1↓, Bcl-2↓, Bcl-xL↓,
799- GAR,    Apoptosis-inducing effect of garcinol is mediated by NF-kappaB signaling in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, NMSC, MCF10
TumCG↓, Apoptosis↑, NF-kB↓,
800- GAR,    Garcinol Regulates EMT and Wnt Signaling Pathways In Vitro and In Vivo, Leading to Anticancer Activity against Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, NA, NA
EMT↓, MET↑, E-cadherin↑, Vim↓, Zeb1↓, ZEB2↑, miR-200c↑, Let-7↑, p‑β-catenin/ZEB1↓, NF-kB↓,
793- GAR,    Garcinol inhibits tumour cell proliferation, angiogenesis, cell cycle progression and induces apoptosis via NF-κB inhibition in oral cancer
- in-vitro, SCC, SCC9 - in-vitro, SCC, SCC4 - in-vitro, SCC, SCC25
TumCG↓, Apoptosis↑, TumCCA↑, NF-kB↓, COX2↓, VEGF↓,
805- GAR,  Cisplatin,  PacT,    Garcinol Exhibits Anti-Neoplastic Effects by Targeting Diverse Oncogenic Factors in Tumor Cells
- Review, NA, NA
ERK↓, PI3K/Akt↓, Wnt/(β-catenin)↓, STAT3↓, NF-kB↓, ChemoSen↑, COX2↓, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, VEGF↓, TGF-β↓, HATs↓, E-cadherin↑, Vim↓, Zeb1↓, ZEB2↓, Let-7↑, MMP9↓, TumCCA↑, ROS↑, MMP↓, IL6↓, NOTCH1↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

PI3K/Akt↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4∅, 1,   HATs↓, 1,   tumCV↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   Let-7↑, 2,   NOTCH1↓, 1,   p‑PI3K↓, 1,   STAT3↓, 2,   TumCG↓, 4,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

E-cadherin↑, 2,   MET↑, 1,   miR-200c↑, 1,   MMP9↓, 1,   TGF-β↓, 2,   TumCP↓, 1,   Vim↓, 2,   Zeb1↓, 2,   ZEB2↓, 1,   ZEB2↑, 1,   p‑β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL6↓, 1,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 8,   ac‑p65↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
8 Garcinol
2 Cisplatin
1 Paclitaxel
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#:83  Target#:214  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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