Garcinol / ROS 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.

Garcinol — a naturally occurring polyisoprenylated benzophenone and polycyclic polyprenylated acylphloroglucinol isolated principally from the dried fruit rind of Garcinia indica, commonly called kokum. It is an experimental phytochemical and pleiotropic epigenetic/signalling modulator, abbreviated GAR and also known as camboginol. Garcinol is best characterized as an inhibitor of lysine and histone acetyltransferases, particularly p300/CBP and PCAF/KAT2B, while also modulating NF-κB, STAT3, PI3K/AKT, inflammatory lipid mediators, apoptosis, and epithelial–mesenchymal plasticity. It is not an approved anticancer drug and should not be equated with whole Garcinia cambogia or hydroxycitric-acid supplements.

Primary mechanisms (ranked):

  1. Inhibition of p300/CBP and PCAF histone acetyltransferase activity, producing broad changes in histone and non-histone protein acetylation, chromatin transcription, DNA-damage responses, and oncogenic gene expression.
  2. Suppression of NF-κB and JAK/Src/STAT3 survival and inflammatory transcription, with reductions in Bcl-2-family proteins, survivin, cyclin D1, VEGF, cytokines, and invasion-associated genes.
  3. Induction of intrinsic and extrinsic apoptosis through mitochondrial membrane-potential loss, cytochrome-c release, Bax/Bcl-2 displacement, caspase activation, DR5 upregulation, and c-FLIP/XIAP suppression.
  4. Suppression of PI3K/AKT/mTOR, FAK/Src/ERK, Wnt/β-catenin, Notch, and cancer-stem-cell signalling in model-dependent settings.
  5. Reversal of epithelial–mesenchymal transition and inhibition of invasion, migration, angiogenesis, and stem-like phenotypes through modulation of E-cadherin, vimentin, ZEB factors, Twist1, MMP-2/9, miR-200-family members, let-7, and related pathways.
  6. Inhibition of inflammatory lipid-mediator enzymes, including 5-lipoxygenase and microsomal prostaglandin E synthase-1, reducing leukotriene and PGE2-associated signalling.
  7. ROS elevation and oxidative-stress-mediated apoptosis in selected cancer models; this is secondary and context-dependent because garcinol can also act as a direct antioxidant or radical scavenger in cell-free and non-cancer systems.
  8. Chemosensitization and radiosensitization through suppression of survival and EMT pathways and, for radiation, inhibition of p300/CBP-dependent non-homologous end joining.

Bioavailability / PK relevance: Garcinol is highly lipophilic and poorly water-soluble, making oral absorption and formulation important translational variables. Rat studies reported approximately 27–36% absolute oral bioavailability at oral doses of 22.5–45 mg/kg, with dose-dependent exposure and substantial tissue distribution. Human liver-microsome data suggest intermediate metabolic clearance, but no validated human cancer PK, therapeutic plasma range, or clinically established dose is available. Nanoparticles, phospholipid complexes, cyclodextrins, and other delivery systems may improve exposure, but remain preclinical.

In-vitro vs systemic exposure relevance: Most anticancer experiments use approximately 5–50 µM garcinol, frequently around 10–25 µM. Whether these free concentrations are safely achievable in human tumors is unknown. Rat PK indicates systemic absorption, but it does not establish sustained human exposure comparable with common cell-culture concentrations. Results obtained at 25–100 µM should therefore be treated as high-concentration or mechanistic findings rather than directly clinically achievable effects.

Clinical evidence status: Preclinical. Evidence consists primarily of biochemical assays, cancer-cell studies, organoid or stem-like-cell models, and rodent xenograft or genetically engineered tumor models. Combination activity has been reported with cisplatin, paclitaxel, gemcitabine, TRAIL, curcumin, and ionizing radiation, but no convincing randomized human oncology trial or established adjunctive anticancer use was identified. Garcinol is not approved by FDA, Health Canada, or EMA as a cancer therapy.

Safety / deployment status: A standardized 40% garcinol preparation showed low acute and repeated-dose toxicity in rodent studies, including a reported 90-day no-observed-adverse-effect level of 100 mg/kg/day. These data do not establish long-term human safety, reproductive safety, drug-interaction risk, or safety during chemotherapy. Garcinol can inhibit platelet activation experimentally and modulates acetyltransferases and multiple drug-relevant signalling pathways, creating plausible interaction concerns. Hepatotoxicity reports involving multi-ingredient Garcinia cambogia supplements cannot be attributed specifically to purified garcinol.

Garcinol Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 HAT and HDAC11 epigenetic regulation p300/CBP HAT ↓; PCAF HAT ↓; HDAC11 ↓; histone and non-histone acetylation altered Acetylation-dependent transcription and differentiation may also be altered P, R, G Epigenetic and transcriptional reprogramming HAT inhibition is the dominant and most established direct mechanism. HDAC11 inhibition is supported by biochemical and cellular evidence but is less broadly characterized. Because HAT and HDAC inhibition can have opposing effects on specific lysine residues, net acetylation changes are substrate-dependent rather than uniformly increased or decreased.
2 NF-κB inflammatory survival signalling NF-κB activation ↓; nuclear p65 signalling ↓; COX-2 ↓; IL-6 ↓; anti-apoptotic genes ↓ Inflammatory activation ↓ (context-dependent) R, G Survival and inflammatory transcription suppression Consistent across several cancer models, although the precise acetylation state of p65 can vary by experimental context.
3 JAK Src STAT3 axis JAK1/2 ↓; Src ↓; STAT3 phosphorylation ↓; STAT3 acetylation and dimerization ↓ Not adequately characterized R, G Oncogenic transcription and survival suppression Reduces cyclin D1, Bcl-2, Bcl-xL, Mcl-1, survivin, and VEGF in responsive models.
4 Mitochondrial apoptosis Bax and Bak ↑; Bcl-2 and Bcl-xL ↓; mitochondrial membrane potential ↓; cytochrome c ↑; caspase-9/3 ↑ Generally weaker effects in tested non-tumorigenic cells (model-dependent) R, G Intrinsic apoptotic cell death Usually downstream of survival-pathway, epigenetic, ER-stress, or oxidative-stress modulation.
5 Death receptor and TRAIL signalling DR5 ↑; c-FLIP ↓; XIAP ↓; survivin ↓; caspase-8 ↑; TRAIL sensitivity ↑ Limited sensitization in tested normal-cell models R, G Extrinsic apoptosis and TRAIL sensitization Combination mechanism; clinical efficacy and selectivity have not been established.
6 PI3K AKT mTOR signalling PI3K phosphorylation ↓; AKT phosphorylation ↓; mTOR phosphorylation ↓ Not adequately characterized R, G Growth and survival inhibition Prominent in gastric, ovarian, colorectal, and other selected models but not necessarily a direct universal target.
7 Cell-cycle checkpoints Cyclin D1 ↓; CDK2/4 ↓; p21 ↑; p27 ↑; G1 or G2 arrest ↑ (model-dependent) Possible cytostatic effects at sufficient exposure G Proliferation arrest Checkpoint outcome varies with tumor genotype, p53 status, dose, and exposure duration.
8 EMT invasion and metastasis E-cadherin ↑; vimentin ↓; Twist1 ↓; ZEB1/2 ↓; MMP-2/9 ↓; migration and invasion ↓ Limited data G Anti-invasive and anti-metastatic phenotype Linked to NF-κB, STAT3, p300, TGF-β, Wnt, and miRNA modulation.
9 Cancer stem-cell signalling ALDH1A1 ↓; OCT4 ↓; SOX2 ↓; Notch1 ↓; Wnt/β-catenin ↓; miR-200c and let-7 ↑ Normal stem-cell effects insufficiently characterized G Stem-like phenotype suppression Supported by cell and xenograft models; potential normal progenitor-cell effects require clarification.
10 Inflammatory lipid mediators 5-lipoxygenase ↓; microsomal prostaglandin E synthase-1 ↓; PGE2 ↓ Inflammatory lipid production ↓ P, R Anti-inflammatory and anti-tumor-promoting activity Direct enzyme inhibition is reported at submicromolar to low-micromolar concentrations and may be relevant independently of HAT inhibition.
11 Mitochondrial ROS and ER stress ROS ↑; GSH ↓; CHOP ↑; mitochondrial stress ↑ (context-dependent) ROS scavenging or antioxidant activity may occur (context-dependent) P, R, G Secondary oxidative-stress-mediated apoptosis Bidirectional redox behaviour is likely determined by concentration, cellular redox state, assay system, and tissue context.
12 Angiogenesis and hypoxic signalling VEGF ↓; HIF-1α ↓; CD31 ↓; angiogenesis ↓ Normal vascular effects insufficiently characterized G Reduced tumor vascular support Often downstream of NF-κB, STAT3, PI3K/AKT, PGE2, and invasion-pathway suppression.
13 Chemosensitization Response to cisplatin, paclitaxel, gemcitabine, and TRAIL ↑ (model-dependent) Combination toxicity inadequately defined G Enhanced treatment response Evidence is preclinical; interaction direction may depend on cancer type, schedule, and chemotherapy mechanism.
14 Radiosensitization and DNA repair p300/CBP-dependent non-homologous end joining ↓; radiation response ↑ Normal-tissue radiosensitization insufficiently characterized R, G Impaired DNA double-strand-break repair Potentially therapeutically relevant but currently supported mainly by cell-based evidence.
15 Clinical Translation Constraint Active concentrations commonly 5–50 µM; tumor exposure unknown Human therapeutic window and interaction profile unknown G Limits clinical interpretation Moderate rat oral bioavailability does not establish achievable human tumor concentrations; formulation, purity, metabolism, and long-term safety remain unresolved.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
821- GAR,    Garcinol inhibits cell growth in hepatocellular carcinoma Hep3B cells through induction of ROS-dependent apoptosis
- in-vitro, Liver, Hep3B
ROS↑, CHOP/DDIT3↑, MMP↓, Bax:Bcl2↑, Casp8↑, Casp3↑, Casp9↑, cl‑PARP↑, DFF45↑,
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↓,
823- GAR,    Garcinol Potentiates TRAIL-Induced Apoptosis through Modulation of Death Receptors and Antiapoptotic Proteins
- in-vitro, BC, MCF7 - in-vitro, Nor, MCF10 - in-vitro, CRC, HCT116
Casp3↑, Casp9↑, Casp8↑, DR5↑, survivin↓, Bcl-2↓, XIAP↓, cFLIP↓, BAX↑, Cyt‑c↑, ROS↑, GSH↓, *eff↓,
820- GAR,    Garcinol in gastrointestinal cancer prevention: recent advances and future prospects
- Review, NA, NA
Fas↑, TRAIL↑, PARP↑, BAX↑, Bcl-2↓, ROS↑, STAT3↓, Apoptosis↑, MMP2↓, MMP9↓,
7087- GAR,    Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential
- Review, Var, NA
HATs↓, p300↓, CBP↓, NF-kB↓, STAT3↓, PI3K↓, Akt↓, MAPK↓, Wnt↓, β-catenin/ZEB1↓, Inflam↓, angioG↓, TumCP↓, TumMeta↓, TumCCA↑, EMT↓, CSCs↓, P53↑, TrxR↓, ROS↑, JNK↑, DNAdam↑, mt-Apoptosis↑, ER Stress↑, CHOP/DDIT3↑, DDIT4↑, TRIB3↑, SESN2↑, miR-218↑, eff↑, ChemoSen↑, BioAv↓, Half-Life↓, BioAv↑,
7092- GAR,    Garcinol and Its Role in Chronic Diseases
- Review, Var, NA
antiOx↑, Inflam↓, AntiCan↑, NF-kB↓, STAT3↓, antiNeop↑, 5LO↓, eff↑, HATs↓, p300↓, PCAF↓, miR-200c↑, NOTCH1↓, CSCs↓, COX2/PTGS2↓, cycD1/CCND1↓, VEGF↓, PI3K↓, Akt↓, Wnt↑, β-catenin/ZEB1↓, ROS↑, CHOP/DDIT3↑, Bax:Bcl2↑, Casp8↑, FAK↓, *neuroP↑, PCNA↓, *GSTs↑,
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/PTGS2↓, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, VEGF↓, TGF-β↓, HATs↓, E-cadherin↑, Vim↓, Zeb1↓, ZEB2↓, Let-7↑, MMP9↓, TumCCA↑, ROS↑, MMP↓, IL6↓, NOTCH1↓, antiNeop↑,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DDIT4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   GSH↓, 1,   ROS↑, 7,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PI3K/Akt↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 1,   mt-Apoptosis↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 2,   Bcl-2↓, 3,   Casp3↑, 3,   Casp8↑, 3,   Casp9↑, 3,   CBP↓, 1,   cFLIP↓, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 1,   JNK↑, 1,   MAPK↓, 1,   survivin↓, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

cSrc↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

HATs↓, 3,   miR-218↑, 1,   PCAF↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 3,   ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

SESN2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DFF45↑, 1,   DNAdam↑, 1,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 2,   EMT↓, 1,   ERK↓, 1,   Let-7↑, 1,   NOTCH1↓, 2,   p300↓, 2,   PI3K↓, 2,   STAT3↓, 5,   TumCG↓, 1,   Wnt↓, 1,   Wnt↑, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   miR-200c↑, 1,   MMP2↓, 1,   MMP9↓, 2,   TGF-β↓, 2,   TRIB3↑, 1,   TumCP↓, 1,   TumMeta↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   IL6↓, 1,   Inflam↓, 2,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 4,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 2,   eff↑, 2,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 2,  
Total Targets: 84

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSTs↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
7 Garcinol
1 Cisplatin
1 Paclitaxel/Taxol
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#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

Home Page