Juglone Cancer Research Results

JG, Juglone: Click to Expand ⟱
Features:
Found in roots, leaves, nut-hulls, bark and wood of walnut trees.
Juglone (5-hydroxy-1,4-naphthoquinone)
Juglans nigra refers to the black walnut tree, which is one of the most well-known sources of juglone
-Research has focused on the hulls (the green outer covering of the walnut) because they have the highest concentrations.
-Fresh hulls can contain juglone levels in the range of approximately 1–5% of the dry weight

-Juglone can redox cycle to generate reactive oxygen species (ROS).
-Increasing Bax, decreasing Bcl‑2, caspase activation, and MMP depolarization.
-Modulation of MAPK pathways (including ERK, JNK, and p38)
-May inhibit NF‑κB signaling
-Cause DNA damage or stress that, in turn, leads to p53 pathway activation— Pin1 Inhibition
–Pin1, a peptidyl-prolyl cis/trans isomerase, is frequently overexpressed in cancer.

-ic50 maybe 5-10uM
-For matching 5uM, crude estimate is 5mg consumption of juglone required which might be 1.5 g of black walnut hull material

Juglone — Juglone (5-hydroxy-1,4-naphthoquinone; JG) is a naturally occurring redox-active naphthoquinone found in plants of the Juglans genus, including black walnut (Juglans nigra), with particularly high concentrations reported in green walnut hulls. It is best classified as a natural small-molecule quinone and experimental anticancer agent rather than an established therapeutic drug. Its anticancer activity is strongly concentration-dependent and reflects electrophilic thiol reactivity, redox cycling, oxidative stress, mitochondrial injury, ferroptosis, apoptosis, and modulation of several oncogenic signaling pathways. Juglone is also widely used experimentally as a Pin1 inhibitor, although this designation should not imply high target selectivity because juglone can covalently modify protein sulfhydryl groups and affect transcription and other cellular proteins.

Primary mechanisms (ranked):

  1. Quinone redox cycling and electrophilic thiol reactivity causing ↑ ROS, ↓ glutathione-dependent antioxidant capacity, oxidative macromolecular injury, and oxidative-stress-driven cell death.
  2. Ferroptosis induction through lipid peroxidation and disruption of antioxidant defenses, including ↓ GPX4 and, in some cancer models, ↓ NRF2 signaling or activation of the FOSL1-HMOX1 axis.
  3. Mitochondrial apoptosis through ↓ mitochondrial membrane potential, ↑ Bax/Bcl-2 ratio, cytochrome-c release, and caspase activation.
  4. Pin1 inhibition contributing to suppression of proliferation, cancer-cell stemness, EMT, migration, angiogenesis, and oncogenic signaling; however, juglone is not a highly selective Pin1 pharmacological probe.
  5. Suppression of PI3K-AKT and related survival signaling, frequently downstream of or amplified by oxidative stress.
  6. Cell-cycle arrest through modulation of cyclins, CDKs, p21, p27, p53, and related checkpoint pathways.
  7. Stress-MAPK modulation, particularly ↑ p38 and ↑ JNK, contributing to apoptosis, ferroptosis, and autophagic responses.
  8. Suppression of EMT, invasion, stem-like phenotype, Wnt/β-catenin signaling, HIF-1α, VEGF, and angiogenic/metastatic programs in selected cancer models.
  9. Autophagy induction as a context-dependent stress response that can interact with apoptosis and oxidative injury.

Bioavailability / PK relevance: Free juglone has unfavorable drug-delivery characteristics, including hydrophobicity, high chemical reactivity, rapid disposition, and substantial renal exposure. In an animal intravenous PK study, free juglone had a plasma half-life of approximately 2 hours and showed prominent kidney localization; sterically stabilized liposomal delivery increased plasma half-life approximately 12-fold, improved tumor localization, and reduced renal toxicity. Robust human oral pharmacokinetic data are lacking. Consequently, dietary or walnut-hull intake cannot presently be converted reliably into a systemic micromolar juglone exposure.

In-vitro vs systemic exposure relevance: Most direct anticancer studies use approximately low-to-tens-of-micromolar juglone, commonly around 5–20 µM. Whether these free-drug concentrations can be maintained safely in human tumors is not established. Recent quantitative work also demonstrates limited intracellular accumulation despite extracellular juglone exposure. Thus, common in-vitro concentrations should not be assumed to be achievable through oral walnut or black-walnut-hull consumption.

Clinical evidence status: Preclinical. Juglone has substantial cell-culture evidence and multiple mouse/xenograft studies showing antitumor activity, including apoptosis, ferroptosis, anti-metastatic, and anti-angiogenic effects. There is no established anticancer dose, regulatory approval, or convincing human clinical efficacy evidence for juglone itself. Translation is limited by nonspecific electrophilic/redox chemistry, systemic toxicity risk, formulation and pharmacokinetic limitations, and the uncertain therapeutic window between cancer and normal tissues.

Juglone Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Quinone redox cycling and thiol reactivity ↑ ROS; ↑ oxidative stress; ↓ cellular thiol buffering ↑ oxidative injury possible P/R Oxidative-stress overload Central upstream mechanism. Juglone participates in redox cycling and can react with protein and glutathione sulfhydryl groups; this contributes to efficacy but also limits selectivity.
2 Glutathione and antioxidant defense ↓ GSH; ↓ GPX4; ↓ SOD (model-dependent) ↓ antioxidant reserve possible (dose-dependent) R Loss of redox buffering Creates a permissive environment for ROS accumulation, lipid oxidation, apoptosis, and ferroptosis.
3 Ferroptosis and lipid peroxidation ↑ ferroptosis; ↑ lipid peroxidation; ↑ MDA; ↑ labile iron Potential ferroptotic toxicity at sufficient exposure R/G Iron-dependent oxidative cell death Strong recent evidence in hepatocellular carcinoma and glioblastoma; pathway execution is cancer-type dependent.
4 NRF2 GPX4 antioxidant axis ↓ NRF2; ↓ GPX4 (model-dependent) Not established R/G Ferroptosis sensitization Demonstrated particularly in glioblastoma. NRF2 modulation should not be generalized to every tumor model.
5 FOSL1 HMOX1 ferroptosis axis ↑ FOSL1; ↑ HMOX1 Not established G Ferroptosis amplification Recent HCC and pan-cancer evidence identifies this transcriptional axis as an important juglone-responsive ferroptotic mechanism.
6 Mitochondrial membrane integrity ↓ membrane potential; ↑ cytochrome-c release Mitochondrial toxicity possible R Intrinsic apoptosis initiation Observed across breast, gastric, prostate, and other cancer models.
7 BAX BCL2 caspase apoptosis ↑ BAX; ↓ BCL2; ↑ caspase-3/7; ↑ caspase-8/9 Apoptosis possible at cytotoxic exposure R/G Programmed cell death Both intrinsic and extrinsic apoptotic pathways can participate. Recent colorectal cancer data support activation of caspase-8 as well as mitochondrial caspase-9 signaling.
8 Pin1 prolyl isomerase ↓ Pin1 activity/function ↓ Pin1 and other thiol-sensitive proteins possible P/R Reduced oncogenic signaling and stemness Important experimental target associated with ↓ proliferation, ↓ EMT, ↓ stemness, and ↓ angiogenesis. Juglone is not Pin1-selective and can directly modify sulfhydryl-containing proteins.
9 PI3K AKT survival signaling ↓ PI3K; ↓ AKT; ↓ p-AKT Context-dependent R/G Survival pathway suppression ROS scavenging can partially reverse this effect in NSCLC, indicating substantial coupling between oxidative stress and PI3K-AKT inhibition.
10 p38 JNK stress signaling ↑ p38; ↑ JNK Context-dependent R Stress-mediated apoptosis and ferroptosis Activation is frequently associated with ROS production and can contribute to NRF2-GPX4 suppression and programmed cell death.
11 Cell cycle checkpoints ↑ arrest; ↓ CDK2; ↓ CDK4; ↓ cyclins; ↑ p21; ↑ p27 Growth inhibition possible G Proliferation blockade Cell-cycle phase varies by model. Recent colorectal cancer data support G0/G1 arrest with suppression of CCND1, CCNB1, CDK2, and CDK4.
12 p53 DNA damage response ↑ DNA damage; ↑ γH2AX; ↑ p53 (model-dependent) Genotoxicity possible R/G Checkpoint activation and apoptosis May arise partly from quinone-driven ROS and electrophilic stress rather than a specific DNA-targeting interaction.
13 Intracellular calcium and mitochondrial stress ↑ Ca²⁺ (model-dependent) Not established P/R Apoptotic signaling Increased intracellular Ca²⁺ has been demonstrated in MCF-7 cells together with ROS elevation and mitochondrial depolarization.
14 EMT migration and invasion ↓ EMT; ↑ E-cadherin; ↓ N-cadherin; ↓ Snail; ↓ migration; ↓ invasion Not established G Reduced metastatic phenotype Pin1, AKT-GSK3β-Snail, TGF-β-related, and other signaling systems have been implicated depending on tumor model.
15 Cancer stemness ↓ sphere formation; ↓ tumor-initiating phenotype Not established G Reduced self-renewal and metastatic potential Pin1 inhibition appears to contribute. Effects have been demonstrated in colorectal and other tumor-initiating cell models.
16 Wnt beta-catenin signaling ↓ Wnt/β-catenin (model-dependent) Not established G Reduced invasion and angiogenesis Most clearly demonstrated in pancreatic cancer models; not necessarily a universal primary mechanism.
17 HIF-1α VEGF angiogenic signaling ↓ HIF-1α; ↓ VEGF; ↓ angiogenesis Potential vascular effects not well characterized G Reduced tumor vascular support Secondary/contextual anticancer mechanism reported in pancreatic cancer and Pin1-related models.
18 Autophagy stress response ↑ LC3-II; ↑ Beclin-1; ↓ p62 (model-dependent) Context-dependent G Autophagic stress and death crosstalk Autophagy can accompany ROS/MAPK signaling but its contribution to net cytotoxicity varies by cell type and experimental conditions.
19 Chemosensitization ↑ drug cytotoxicity in selected combinations Potential ↑ combination toxicity G Combination-treatment sensitization Juglone can enhance etoposide cytotoxicity through Pin1-related mechanisms, but sequence of administration can substantially alter the interaction.
20 Clinical Translation Constraint Effective concentrations commonly ~5–20 µM in vitro Systemic electrophilic and oxidative toxicity limits selectivity G Uncertain therapeutic window Human bioavailability and therapeutic exposure are not established. Free juglone has short animal plasma persistence, renal accumulation, and nephrotoxicity; formulations such as liposomes materially alter PK and distribution.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr

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Scientific Papers found: Click to Expand⟱
7965- JG,    Mechanistic investigation of Juglone (5-hydroxy-1,4-naphthoquinone) as an anti-cancer agent in human colorectal cancer HCT116 and HT-29 cell lines
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT-29
Apoptosis↑, Casp3↑, Casp7↑, Casp8↑, Casp9↑, Bcl-2↓, TumCCA↑, cycD1/CCND1↓, CycB/CCNB1↓, CDK2↓, CDK4↓, ERK↓, AKT1↓, p38↑, JNK↑, TumCMig↓, TumCI↓, TumMeta↓,
5118- JG,    Juglone induces apoptosis and autophagy via modulation of mitogen-activated protein kinase pathways in human hepatocellular carcinoma cells
- in-vitro, HCC, HepG2
m-ROS↑, DNAdam↑, Apoptosis↑, TumAuto↑, p38↑, MAPK↑, JNK↑, MMP↓, LC3II↑, Beclin-1↑,
5119- JG,    Juglone Suppresses Inflammation and Oxidative Stress in Colitis Mice
- in-vivo, Nor, NA
*antiOx↑, *OS↑, *IL6↓, *IL12↓, *IL23↓, *TNF-α↓, *Inflam↓, *NF-kB↓, *NFE2L2↓, *ROS↓,
5120- JG,    Juglone can inhibit angiogenesis and metastasis in pancreatic cancer cells by targeting Wnt/β-catenin signaling
- in-vitro, PC, NA
angioG↓, Wnt↓, VEGF↓,
7819- JG,    Evaluation of pharmacokinetic, biodistribution, pharmacodynamic, and toxicity profile of free juglone and its sterically stabilized liposomes
- vitro+vivo, Nor, NA
*Half-Life⇅, eff↑, eff↑, Dose↝,
7820- JG,    Juglone, an inhibitor of the peptidyl-prolyl isomerase Pin1, also directly blocks transcription
Pin1↓,
7961- JG,    Juglone Inhibits Tumor Metastasis by Regulating Stemness Characteristics and the Epithelial-to-Mesenchymal Transition in Cancer Cells both in Vitro and in Vivo
- vitro+vivo, BC, MCF7 - in-vitro, BC, 4T1 - vitro+vivo, CRC, HCT116
EMT↓, CSCs↓, TumMeta↓, Pin1↓, TumCCA↑, angioG↓, Apoptosis↑, BAX↑, Bcl-2↓,
7962- JG,    Peptidyl prolyl isomerase, Pin1 is a potential target for enhancing the therapeutic efficacy of etoposide
- in-vitro, Var, NA
eff↑, Pin1↓, *DNAdam↓,
7963- JG,    Pin1 Inhibitor Juglone Exerts Anti-Oncogenic Effects on LNCaP and DU145 Cells despite the Patterns of Gene Regulation by Pin1 Differing between These Cell Lines
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, DU145
Pin1↓, TumCP↓, TumVol↓, other↝,
7964- JG,    Juglone and KPT6566 Suppress the Tumorigenic Potential of CD44+CD133+ Tumor-Initiating Caco-2 Cells In Vitro and In Vivo
- vitro+vivo, Colon, Caco-2
CSCs↓, TumVol↓, Pin1↓,
5117- JG,    https://pubmed.ncbi.nlm.nih.gov/31283929/
- vitro+vivo, Liver, NA
TumCG↓, TumCP↓, Apoptosis↑, TumAuto↑, AMPK↑, mTOR↑, P53↑, H2O2↑, ROS↑,
7966- JG,    Discovery of Juglone Derivatives as Novel STAT3 Inhibitors with Potent Suppression of Cancer Cell Stemness against Breast Cancer
- in-vitro, BC, NA
STAT3↓, CSCs↓,
8002- JG,    Identification and Biological Evaluation of Juglone-Derived STAT3 Inhibitors against Colorectal Cancer
- in-vitro, PC, NA - in-vitro, CRC, NA
eff↑, STAT3↓, TumCP↓, selectivity↑,
8003- JG,  doxoR,    A juglone derivative that disrupts mitochondrial redox metabolism, inhibiting the breast fibroblast-cancer cell pro-migratory signaling induced by doxorubicin
- in-vitro, BC, NA
TumCP↓, TumCCA↑, mt-NADH↑, mt-OCR↑, mt-SOD2↑,
8004- JG,    TP53 Is a Potential Target of Juglone Against Colorectal Cancer: Based on a Combination of Molecular Docking, Molecular Dynamics Simulation, and In Vitro Experiments
*Inflam↓, *AntiViral↑, *AntiCan↑, ROS↑, P53↑, TumCP↓,
8005- JG,    Immunomodulation by juglone alleviates acute graft-versus-host disease without compromising the graft-versus-leukaemia activity in mice
- in-vivo, AML, NA
DCells↓, CD4+↓, OS↑, Imm↝,
8006- JG,  VitC,    Juglone-ascorbate treatment enhances reactive oxygen species mediated mitochondrial apoptosis in pancreatic cancer
- in-vitro, PC, PANC1 - in-vitro, PC, Bxpc-3
TumCP↓, ROS↑, antiOx⇅, Bcl-2↓, survivin↓, BAX↑, Trx2↓, eff↑,
8007- JG,    Juglone reduces growth and migration of U251 glioblastoma cells and disrupts angiogenesis
- in-vitro, GBM, U251
Pin1↓, AntiCan↑, TumCP↓, Apoptosis↑, Casp3↑, TumCMig↓, angioG↓, VEGF↓, CD31/PECAM-1↓, TGF-β1↓,
8008- JG,    Juglone, isolated from Juglans mandshurica Maxim, induces apoptosis via down-regulation of AR expression in human prostate cancer LNCaP cells
- in-vitro, NA, LNCaP
TumCG↓, MMP↓, Casp3↑, AR↓, PSA↓,
1925- JG,    Redox regulation of mitochondrial functional activity by quinones
- in-vitro, NA, NA
other↓, ROS↑, MMP↓, eff↝,
1121- JG,    Juglone suppresses epithelial-mesenchymal transition in prostate cancer cells via the protein kinase B/glycogen synthase kinase-3β/Snail signaling pathway
- in-vitro, Pca, LNCaP
E-cadherin↑, N-cadherin↓, Vim↓, Snail↓, GSK‐3β↑,
1917- JG,    Inhibition of human leukemia cells growth by juglone is mediated via autophagy induction, endogenous ROS production, and inhibition of cell migration and invasion
- in-vitro, AML, HL-60
selectivity↑, LC3I↑, LC3II↑, Beclin-1↑, ROS↑, tumCV↓, Dose↝, TumAuto↑,
1918- JG,    ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro
- in-vitro, Liver, HepG2 - in-vivo, NA, NA
TumCG↓, TumCP↓, Apoptosis↑, TumAuto↑, AMPK↑, mTOR↑, P53↑, H2O2↑, ROS↑, toxicity↝, p62↓, DR5↑, Casp8↑, PARP↑, cl‑Casp3↑,
1919- JG,    The Anti-Glioma Effect of Juglone Derivatives through ROS Generation
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
ROS↑, Apoptosis↑, eff↓, eff↓,
1920- JG,  TQ,  PLB,    Natural quinones induce ROS-mediated apoptosis and inhibit cell migration in PANC-1 human pancreatic cancer cell line
- in-vitro, PC, PANC1
ROS↑, TumCMig↓, MMP9↓,
1921- JG,    Juglone induces ferroptotic effect on hepatocellular carcinoma and pan-cancer via the FOSL1-HMOX1 axis
- in-vitro, PC, NA - vitro+vivo, PC, NA
TumCG↓, Ferroptosis↑, ROS↑, Iron↑, lipid-P↑, MDA↑, GSH↓, FOSL1↑, HO-1↑,
1922- JG,    Juglone induces apoptosis of tumor stem-like cells through ROS-p38 pathway in glioblastoma
- in-vitro, GBM, U87MG
tumCV↓, TumCP↓, ROS↑, p‑p38↑, eff↓, Apoptosis↑, OS↑,
1923- JG,    Mechanism of Juglone-Induced Cell Cycle Arrest and Apoptosis in Ishikawa Human Endometrial Cancer Cells
- in-vitro, Endo, NA
TumCP↓, TumCCA↑, cycA1/CCNA1↓, ROS↑, P21↑, CDK2↓, CDK1↓, CDC25↓, Bcl-2↓, Bcl-xL↓, BAX↑, BAD↑, Cyt‑c↑,
1924- JG,    Juglone triggers apoptosis of non-small cell lung cancer through the reactive oxygen species -mediated PI3K/Akt pathway
- in-vitro, Lung, A549
TumCMig↓, TumCI↓, TumCCA↑, Apoptosis↑, cl‑Casp3↑, BAX↑, Cyt‑c↑, ROS↑, MDA↑, GPx4↓, SOD↓, PI3K↓, Akt↓, eff↓,
974- JG,    Juglone down-regulates the Akt-HIF-1α and VEGF signaling pathways and inhibits angiogenesis in MIA Paca-2 pancreatic cancer in vitro
- in-vitro, PC, MIA PaCa-2
Hif1a↓, VEGF↓, p‑Akt↓, TumCP↓, TumCI↓,
1926- JG,    Mechanism of juglone-induced apoptosis of MCF-7 cells by the mitochondrial pathway
- in-vitro, BC, MCF7
TumCG↓, ROS↑, MMP↓, i-Ca+2↑, BAX↑, Bcl-2↓, Cyt‑c↑, Casp3?,
1927- JG,    Juglone-induced apoptosis in human gastric cancer SGC-7901 cells via the mitochondrial pathway
- in-vitro, GC, SGC-7901
Apoptosis↑, ROS↑, Bcl-2↓, BAX↑, MMP↓, Cyt‑c↑, Casp3?, Bax:Bcl2↑,
5098- JG,    Effects of Juglone on Antioxidant Status in Pancreatic Cancer Cell Lines
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
tumCV↓, ROS↑, GSH⇅,
5099- JG,    Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK
- vitro+vivo, GBM, LN229 - vitro+vivo, GBM, T98G
Ferroptosis↑, p‑MAPK↑, NRF2↓, GPx4↓, TumPF↓, Apoptosis↑, ROS↑, GSH↓, lipid-P↑, Ki-67↓, TumCG↓,
5113- JG,    Juglone in Oxidative Stress and Cell Signaling
- Review, Var, NA - Review, AD, NA
ROS↑, Pin1↓, antiOx⇅, *ROS↓, SMAD2↓, GSH↓, lipid-P↑, TumCCA↓, BAX↑, Bcl-2↓, Casp3↑, Casp9↑, Ca+2↑, Cyt‑c↑, AntiFungal↑, Bacteria↓, Akt↓,
5114- JG,    Juglone, from Juglans mandshruica Maxim, inhibits growth and induces apoptosis in human leukemia cell HL-60 through a reactive oxygen species-dependent mechanism
- in-vitro, AML, HL-60
ROS↑, GSH↓, eff↓, cl‑PARP↑, proCasp3↑, proCasp9↑, MMP↓, Cyt‑c↑, Diablo↑,
5115- JG,    Natural Products to Fight Cancer: A Focus on Juglans regia
- Review, Var, NA
Casp3↑, Casp9↑, MMP↓, AR↓, PSA↓, E-cadherin↑, N-cadherin↓, Vim↓, Akt↓, GSK‐3β↓, EMT↑, TumCI↓, MMP9↓, VEGF↓, MMP2↓, TumCCA↑, ROS↑, Apoptosis↑, GSH↓, Catalase↓, SOD↓, GPx↓, DNAdam↑, γH2AX↑, eff↑, BAX↑, Fas↑, Pin1↓,
5116- JG,    Juglone, a naphthoquinone from walnut, exerts cytotoxic and genotoxic effects against cultured melanoma tumor cells
- in-vitro, Melanoma, B16-BL6
GSH↓, ROS↑, chemoPv↑,

Showing Research Papers: 1 to 38 of 38

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 38

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx⇅, 2,   Catalase↓, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx4↓, 2,   GSH↓, 6,   GSH⇅, 1,   H2O2↑, 2,   HO-1↑, 1,   Iron↑, 1,   lipid-P↑, 3,   MDA↑, 2,   mt-NADH↑, 1,   NRF2↓, 1,   ROS↑, 20,   m-ROS↑, 1,   SOD↓, 2,   mt-SOD2↑, 1,   Trx2↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   MMP↓, 7,   mt-OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AKT1↓, 1,   AMPK↑, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   p‑Akt↓, 1,   Apoptosis↑, 12,   BAD↑, 1,   BAX↑, 8,   Bax:Bcl2↑, 1,   Bcl-2↓, 7,   Bcl-xL↓, 1,   Casp3?, 2,   Casp3↑, 5,   cl‑Casp3↑, 2,   proCasp3↑, 1,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 3,   proCasp9↑, 1,   Cyt‑c↑, 6,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 2,   JNK↑, 2,   MAPK↑, 1,   p‑MAPK↑, 1,   p38↑, 2,   p‑p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   other↝, 1,   tumCV↓, 3,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 2,   LC3I↑, 1,   LC3II↑, 2,   p62↓, 1,   TumAuto↑, 4,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 2,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↓, 1,   TumCCA↑, 6,  

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

CSCs↓, 3,   EMT↓, 1,   EMT↑, 1,   ERK↓, 1,   FOSL1↑, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   mTOR↑, 2,   PI3K↓, 1,   STAT3↓, 2,   TumCG↓, 6,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   i-Ca+2↑, 1,   CD31/PECAM-1↓, 1,   E-cadherin↑, 2,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 2,   SMAD2↓, 1,   Snail↓, 1,   TGF-β1↓, 1,   TumCI↓, 4,   TumCMig↓, 4,   TumCP↓, 11,   TumMeta↓, 2,   TumPF↓, 1,   Vim↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 3,   Hif1a↓, 1,   VEGF↓, 4,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   DCells↓, 1,   Imm↝, 1,   PSA↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,   eff↓, 5,   eff↑, 6,   eff↝, 1,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 2,   Ki-67↓, 1,   PSA↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoPv↑, 1,   OS↑, 2,   Pin1↓, 8,   toxicity↝, 1,   TumVol↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   Bacteria↓, 1,  
Total Targets: 126

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   NFE2L2↓, 1,   ROS↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL12↓, 1,   IL23↓, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Half-Life⇅, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   OS↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,  
Total Targets: 15

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

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