Garcinol 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
Scientific Papers found: Click to Expand⟱
5792- CRMs,  HCA,  CUR,  EGCG,  GAR  Caloric restriction mimetics: natural/physiological pharmacological autophagy inducers
- Review, Nor, NA
*CRM↓, *Dose?, *AntiAge↑, *Acetyl-CoA↓, *SIRT1↑, *AMPK↑, *mTORC1↓, *AntiAge↑, chemoP↑,
1636- GAR,    Dangerous dietary supplements: Garcinia cambogia-associated hepatic failure requiring transplantation
- Case Report, Obesity, NA
*Dose∅, *other↑,
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↓,
824- GAR,    Garcinol A Novel Inhibitor of Platelet Activation and Apoptosis
- in-vitro, NA, NA
AntiAg↓,
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↓,
826- GAR,    Inhibition of STAT3 dimerization and acetylation by garcinol suppresses the growth of human hepatocellular carcinoma in vitro and in vivo
- vitro+vivo, HCC, HepG2 - vitro+vivo, Liver, HUH7
STAT3↓, TumCP↓, cycD1/CCND1↓, Bcl-2↓, Bcl-xL↓, Mcl-1↓, survivin↓, VEGF↓, TumCCA↑, TumVol↓,
827- GAR,    Garcinol Is an HDAC11 Inhibitor
- in-vitro, NA, NA
HDAC11↓,
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↓,
829- GAR,    The Role of T-Cadherin (CDH13) in Treatment Options with Garcinol in Melanoma
- vitro+vivo, Melanoma, NA

830- GAR,    Garcinol modulates tyrosine phosphorylation of FAK and subsequently induces apoptosis through down-regulation of Src, ERK, and Akt survival signaling in human colon cancer cells
- in-vitro, CRC, HT-29
TumCI↓, TumCMig↓, Apoptosis↑, p‑FAK↓, Src↓, MAPK↓, ERK↓, PI3K/Akt↓, Bax:Bcl2↑, Cyt‑c↑, MMP7↓,
831- GAR,  CUR,    Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells
- in-vitro, AML, HL-60
Apoptosis↑, Casp3↑, MMP↓, Cyt‑c↑, proCasp9↑, Bcl-2↓, BAX↑, PARP↓, DNAdam↑, DFF45↓,
832- GAR,  Rad,    Garcinol, a Histone Acetyltransferase Inhibitor, Radiosensitizes Cancer Cells by Inhibiting Non-Homologous End Joining
- in-vitro, Lung, A549 - in-vitro, NA, HeLa
HATs↓, other↑,
1632- GAR,    Garcinia Cambogia, Either Alone or in Combination with Green Tea Causes Moderate to Severe Liver Injury
- Human, LiverDam, NA
HLA↑, other↑,
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↓,
7084- GAR,    A unique in vivo pharmacokinetic profile, in vitro metabolic stability and hepatic first-pass metabolism of garcinol, a promising novel anticancer phytoconstituent, by liquid chromatography–mass spectrometry
- in-vivo, Nor, NA
*BioAv↝, *Dose↝, *Inflam↓, *antiOx↑, *chemoPv↑, Wnt↓, β-catenin/ZEB1↓, ERK↓, PI3K↓, Akt↓, NF-kB↓, STAT3↓, TumCP↓, antiNeop↑, ChemoSen↑, chemoP↑,
7085- GAR,    Safety profile of 40% Garcinol from Garcinia indica in experimental rodents
- in-vivo, Nor, NA
*Dose↓, *toxicity↓,
7086- GAR,    Garcinol: An emerging epigenetic modifier with versatile anticancer properties
- Review, Var, NA
AntiCan↑, TumCG↓, TumMeta↓, toxicity↓, Apoptosis↑, angioG↓, *BioAv↝, HATs↓, p300↓, CBP↓, PI3K↓, Akt↓, NF-kB↓, STAT↓, mTOR↓, DFF45↓, survivin↓, N-cadherin↓, Twist↓, MMP2↓, MMP3↓, MMP9↓, Mcl-1↓, EZH2↓, NOTCH↓, CXCR4↓, PGE2↓, VEGF↓, mPGES-1↓, CycB/CCNB1↓, CDK2↓, CDK4/6↓, iNOS↓, COX2↓, IL1↓, TNF-α↓, PARP↑, Bcl-2↓,
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↑,
7088- GAR,    Garcinol inhibits tumour cell proliferation, angiogenesis, cell cycle progression and induces apoptosis via NF-κB inhibition in oral cancer
- in-vitro, SCC, SCC4
TumCG↓, TumCP↓, Apoptosis↑, TumCCA↑, selectivity↑, NF-kB↓, COX2↓, VEGF↓,
7089- GAR,    Anticancer action of garcinol in vitro and in vivo is in part mediated through inhibition of STAT-3 signaling
- vitro+vivo, BC, MDA-MB-231 - in-vitro, Pca, DU145 - in-vitro, PC, NA
STAT3↓, TumCI↓, NF-kB↓, uPA↓, VEGF↓, MMP9↓,
7090- GAR,    Garcinol
AChE↓, BChE↓, *Inflam↓, *5LO↓, *PGE2↓, *antiOx↑, FAK↓, DNAdam↑, MMP↓, Casp↑, NF-kB↓, HATs↓, *toxicity↓,
7091- GAR,    Garcinol-A Natural Histone Acetyltransferase Inhibitor and New Anti-Cancer Epigenetic Drug
- Review, Var, NA
antiOx↑, Inflam↓, HATs↓, p300↓, CBP↓, PCAF↓, cycD1/CCND1↓, STAT↓, PI3K↓, Akt↓, TumCP↓, TumCI↓, TumMeta↓, TumCCA↑, CDK2↓, CDK4↓,
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↓, cycD1/CCND1↓, VEGF↓, PI3K↓, Akt↓, Wnt↑, β-catenin/ZEB1↓, ROS↑, CHOP/DDIT3↑, Bax:Bcl2↑, Casp8↑, FAK↓, *neuroP↑, PCNA↓, *GSTs↑,
7093- GAR,    Garcinol
- Review, AD, NA
*AChE↓, *BChE↓, *HATs↓, *Inflam↓, AntiCan↑,
7094- GAR,    A multi-targeted approach of garcinol for obesity intervention: Mechanistic insights and possible clinical applications
- Review, Nor, NA
*Obesity↓, *Appetite↓, *GutMicro↑, BioAv↝,
807- GAR,    Garcinol inhibits cell proliferation and promotes apoptosis in pancreatic adenocarcinoma cells
- in-vitro, PC, PANC1 - in-vitro, PC, Bxpc-3
TumCG↓, Apoptosis↑, TumCCA↑,
794- GAR,    Garcinol Enhances TRAIL-Induced Apoptotic Cell Death through Up-Regulation of DR5 and Down-Regulation of c-FLIP Expression
- in-vitro, RCC, NA - in-vitro, Lung, A549 - in-vitro, Nor, NA
DR5↑, cFLIP↓, *toxicity↓,
795- GAR,    Garcinol—A Natural Histone Acetyltransferase Inhibitor and New Anti-Cancer Epigenetic Drug
- Review, NA, NA
HATs↓, BAX↑, PARP↑, Bcl-2↓, Casp3↑, Casp9↑, DR5↑, cFLIP↓, MMP2↓, MMP9↓, STAT3↓, p‑Akt↓,
796- GAR,    Polyisoprenylated benzophenone, garcinol, a natural histone acetyltransferase inhibitor, represses chromatin transcription and alters global gene expression
- vitro+vivo, Pca, HeLa
HATs↓, PCAF↓, Apoptosis↑,
797- GAR,  CUR,    Differential effects of garcinol and curcumin on histone and p53 modifications in tumour cells
- in-vitro, BC, MCF7 - in-vitro, OS, U2OS - in-vitro, OS, SaOS2
TumCP↓, H3K18↓, DNAdam↑,
798- GAR,    Garcinol, an acetyltransferase inhibitor, suppresses proliferation of breast cancer cell line MCF-7 promoted by 17β-estradiol
- in-vitro, BC, MCF7
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, MCF7 - 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↓,
801- GAR,  Cisplatin,    Garcinol sensitizes human head and neck carcinoma to cisplatin in a xenograft mouse model despite downregulation of proliferative biomarkers
- in-vivo, HNSCC, NA
Apoptosis↑, cycD1/CCND1↓, Bcl-2↓, survivin↓, VEGF↓, TumCG↓, Ki-67↓, CD31↓,
802- GAR,    Garcinol acts as an antineoplastic agent in human gastric cancer by inhibiting the PI3K/AKT signaling pathway
- in-vitro, GC, HGC27
TumCP↓, TumCI↓, Apoptosis↑, PI3K/Akt↓, Akt↓, p‑mTOR↓, cycD1/CCND1↓, MMP2↓, MMP9↓, BAX↑, Bcl-2↓,
803- GAR,    Induction of p21(Waf1/Cip1) by garcinol via downregulation of p38-MAPK signaling in p53-independent H1299 lung cancer
- in-vitro, Lung, H1299 - in-vitro, Lung, H460
TumCP↓, TumCCA↑, CDK2↓, CDK4↓, cycD1/CCND1↓, CycD3↓, cycE/CCNE↑, CDK6↑, P21↑, p27↑, ERK↓, MAPK↓,
804- GAR,    Garcinol inhibits the proliferation of endometrial cancer cells by inducing cell cycle arrest
- in-vitro, EC, HEC1B - in-vitro, EC, ISH
TumCP↓, TumCCA↑, P53↑, P21↑, CDK2↓, CDK4↓, cycD1/CCND1↓, CycB/CCNB1↓, p‑cJun↑,
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↓, antiNeop↑,
806- GAR,    Garcinol exerts anti-cancer effect in human cervical cancer cells through upregulation of T-cadherin
- vitro+vivo, Pca, HeLa - vitro+vivo, Cerv, SiHa
TumCI↓, TumCMig↓, TumCCA↑, Apoptosis↑, T-cadherin↑,
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↓,
808- GAR,  CUR,    Synergistic effect of garcinol and curcumin on antiproliferative and apoptotic activity in pancreatic cancer cells
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
tumCV↓, Apoptosis↑, Casp3↑, Casp9↑,
809- GAR,    High-Throughput Screen of Natural Product Libraries for Hsp90 Inhibitors
- Review, NA, NA
HRI↓, HSP90↓,
810- GAR,  GEM,    Garcinol sensitizes human pancreatic adenocarcinoma cells to gemcitabine in association with microRNA signatures
- in-vitro, PC, NA
TumCP↓, Apoptosis↑, PARP↝, VEGF↝, MMPs↝, Casp↝, NF-kB↝, miR-21↝,
811- GAR,    Garcinol exhibits anti-proliferative activities by targeting microsomal prostaglandin E synthase-1 in human colon cancer cells
- in-vitro, CRC, HT-29
mPGES-1↓, Hif1a↓, VEGF↓, CXCR4↓, MMP2↓, MMP9↓, Casp3↑, TumCP↓, PGE2↓,
812- GAR,    Anti-proliferative and anti-invasive effects of garcinol from Garcinia indica on gallbladder carcinoma cells
- in-vitro, Gall, GBC-SD - in-vitro, Gall, NOZ
TumCG↓, TumCI↓, MMP2↓, MMP9↓,
813- GAR,  GEM,    Dietary Garcinol Arrests Pancreatic Cancer in p53 and K-ras Conditional Mutant Mouse Model
- in-vivo, PC, NA
TumCG↓, OS↑,
814- GAR,  PacT,    Garcinol sensitizes breast cancer cells to Taxol through the suppression of caspase-3/iPLA2 and NF-κB/Twist1 signaling pathways in a mouse 4T1 breast tumor model
- in-vivo, BC, NA
Apoptosis↑, TumCCA↑, EMT↓, TumCI↓,
815- GAR,    Garcinol from Garcinia indica Downregulates Cancer Stem-like Cell Biomarker ALDH1A1 in Nonsmall Cell Lung Cancer A549 Cells through DDIT3 Activation
- vitro+vivo, Lung, A549
ALDH1A1↓, CHOP/DDIT3↑,

Showing Research Papers: 1 to 50 of 54
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 54

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DDIT4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   GSH↓, 1,   ROS↑, 7,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 4,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PI3K/Akt↓, 3,  

Cell Death(tgid=5) ⓘ

Akt↓, 6,   p‑Akt↓, 2,   Apoptosis↑, 17,   mt-Apoptosis↑, 1,   BAX↑, 7,   Bax:Bcl2↑, 3,   Bcl-2↓, 10,   Bcl-xL↓, 2,   Casp↑, 1,   Casp↝, 1,   Casp3↑, 7,   cl‑Casp3↑, 1,   Casp8↑, 3,   Casp9↑, 5,   proCasp9↑, 1,   CBP↓, 3,   cFLIP↓, 3,   Cyt‑c↑, 3,   DR5↑, 3,   Fas↑, 1,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 3,   Mcl-1↓, 2,   p27↑, 1,   survivin↓, 4,   TRAIL↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

cSrc↓, 1,   H3K18↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

p‑cJun↑, 1,   EZH2↓, 1,   ac‑H3↑, 1,   ac‑H4∅, 1,   HATs↓, 9,   miR-21↝, 1,   miR-218↑, 1,   other↑, 2,   PCAF↓, 3,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 4,   ER Stress↑, 1,   HRI↓, 1,   HSP90↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

SESN2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DFF45↓, 2,   DFF45↑, 1,   DNAdam↑, 4,   P53↑, 2,   PARP↓, 1,   PARP↑, 3,   PARP↝, 1,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 4,   CDK4↓, 3,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 8,   CycD3↓, 1,   cycE/CCNE↑, 1,   P21↑, 2,   TumCCA↑, 12,  

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

ALDH1A1↓, 1,   CSCs↓, 2,   EMT↓, 3,   ERK↓, 4,   HDAC11↓, 1,   Let-7↑, 2,   mTOR↓, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 2,   p300↓, 4,   PI3K↓, 5,   p‑PI3K↓, 1,   Src↓, 1,   STAT↓, 2,   STAT3↓, 9,   TumCG↓, 10,   Wnt↓, 2,   Wnt↑, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   AntiAg↓, 1,   CD31↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 2,   FAK↓, 2,   p‑FAK↓, 1,   HLA↑, 1,   Ki-67↓, 1,   MET↑, 1,   miR-200c↑, 2,   MMP2↓, 6,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 8,   MMPs↝, 1,   N-cadherin↓, 1,   T-cadherin↑, 1,   TGF-β↓, 2,   TRIB3↑, 1,   TumCI↓, 7,   TumCMig↓, 2,   TumCP↓, 12,   TumMeta↓, 3,   Twist↓, 1,   uPA↓, 1,   Vim↓, 2,   Zeb1↓, 2,   ZEB2↓, 1,   ZEB2↑, 1,   β-catenin/ZEB1↓, 3,   p‑β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   Hif1a↓, 1,   VEGF↓, 9,   VEGF↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 5,   CXCR4↓, 2,   IL1↓, 1,   IL6↓, 1,   Inflam↓, 3,   JAK1↓, 1,   JAK2↓, 1,   mPGES-1↓, 2,   NF-kB↓, 15,   NF-kB↝, 1,   ac‑p65↑, 1,   PGE2↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 3,   eff↑, 2,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,   IL6↓, 1,   Ki-67↓, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   antiNeop↑, 3,   chemoP↑, 2,   OS↑, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 158

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   GSTs↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Acetyl-CoA↓, 1,   AMPK↑, 1,   CRM↓, 1,   SIRT1↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

HATs↓, 1,   other↑, 1,  

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

mTORC1↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 3,   PGE2↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 2,   Dose?, 1,   Dose↓, 1,   Dose↝, 1,   Dose∅, 1,   eff↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   Appetite↓, 1,   chemoPv↑, 1,   neuroP↑, 1,   Obesity↓, 1,   toxicity↓, 3,  
Total Targets: 27

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#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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