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
Scientific Papers found: Click to Expand⟱
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↓, juglone significantly decreased the level of HIF-1α compared to the untreated control
VEGF↓, juglone significantly inhibited VEGF expression in MIA Paca-2 cells
p‑Akt↓, juglone by itself is very effective in inhibiting p-Akt at 5μM in pancreatic cancer MIA Paca-2 cells
TumCP↓,
TumCI↓,

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↑, prevented inactivation

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↑, revealed significant, selective (less cytotoxicity towards normal cells) and dose-dependent inhibition of HL-60 leukemia cells
LC3I↑, significant increase in LC3-I and LC3-II
LC3II↑,
Beclin-1↑, slight increase in Beclin-I
ROS↑, Confocal microscopy revealed tremendous increase in ROS concentrations in a dose-dependent manner
tumCV↓,
Dose↝, ROS percentage was 8%, with 20 μM dose it was 25% and with 80 μM its highest value was observed. dose-dependent increase in ROS production
TumAuto↑, The growth inhibitory effects of juglone were mediated via autophagy induction, endogenous ROS production, and inhibition of cell migration and invasion.

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↓, JG significantly inhibited tumor growth in vivo
TumCP↓, JG effectively inhibited cell proliferation and induced apoptosis through extrinsic pathways
Apoptosis↑,
TumAuto↑, JG treatment induced autophagy flux
AMPK↑, activiting the AMPK-mTOR signaling pathway
mTOR↑,
P53↑, JG enhanced p53 activation
H2O2↑, JG enhanced the generation of hydrogen peroxide (H2O2)
ROS↑, JG caused apoptosis and autophagy via activating the ROS-mediated p53 pathway in human liver cancer cells in vitro and in vivo
toxicity↝, a slight loss in body weight was observed after JG injection (Fig. 1D), suggesting that JG might has slight side effects.
p62↓, rmarkable decrease of p62 level was observed after 30uM JG treatment
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 rates were increased after D2 or D3 treatment via ROS generation
Apoptosis↑,
eff↓, The peak of juglone could be detected in fresh solution (Molecular Weight: 174kD), while many unknown compounds could be found, and juglone itself decreased obviously after oxidation (1 week)
eff↓, NAC, a ROS scavenger, reversed the cytotoxic effect, indicating the involvement of ROS generation in the anti-glioma effect of D2 and D3

1920- JG,  TQ,  Plum,    Natural quinones induce ROS-mediated apoptosis and inhibit cell migration in PANC-1 human pancreatic cancer cell line
- in-vitro, PC, PANC1
ROS↑, thymoquinone, plumbagin and juglone were evaluated for their influence on reactive oxygen species (ROS) generation through 2,7-dichlorofluorescein diacetate (DCFDA) staining and they dramatically increased the intracellular ROS level in treated PANC-
TumCMig↓, inhibited PANC-1 cell migration
MMP9↓, reduced expression of matrix metalloproteinase-9 (MMP-9) in juglone-treated cells

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↓, Juglone suppressed HCC growth via ferroptosis in vitro and in vivo
Ferroptosis↑,
ROS↑, evidenced by increased levels of iron, lipid peroxidation (LPO), reactive oxygen species (ROS), malondialdehyde (MDA)
Iron↑,
lipid-P↑,
MDA↑,
GSH↓, decreased levels of glutathione (GSH)
FOSL1↑, induce ferroptosis in pan-cancer by activating the FOSL1-HMOX1 axis
HO-1↑, HMOX1

1922- JG,    Juglone induces apoptosis of tumor stem-like cells through ROS-p38 pathway in glioblastoma
- in-vitro, GBM, U87MG
tumCV↓, inhibit the proliferation of TSCs in glioma by decreasing cell viability
TumCP↓,
ROS↑, juglone could generate ROS significantly
p‑p38↑, increase p38 phosphorylation
eff↓, pretreatment with ROS scavenger or p38-MAPK inhibitor could reverse juglone-induced cytotoxicity
Apoptosis↑, Juglone could induce glioma stem-like cells apoptosis
OS↑, juglone could increase the survival time by about 23.6%(though less significant than TMZ)

1923- JG,    Mechanism of Juglone-Induced Cell Cycle Arrest and Apoptosis in Ishikawa Human Endometrial Cancer Cells
- in-vitro, Endo, NA
TumCP↓, juglone significantly inhibited Ishikawa cell proliferation
TumCCA↑, as shown by S phase arrest
cycA1↓, inactivation of cyclin A protein
ROS↑, The ROS levels increased significantly after exposure to juglone
P21↑, paralleled increases in the mRNA and protein expression of p21
CDK2↓, decreases in the levels of CDK2, cdc25A, CHK1, and cyclin A
CDK1↓,
CDC25↓,
Bcl-2↓, expression of Bcl-2 and Bcl-xL was significantly down-regulated,
Bcl-xL↓,
BAX↑, expression of Bax, Bad and cyto c was up-regulated
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↓, substantially suppressed the migration and invasion of these two lung cancer cells
TumCI↓,
TumCCA↑, juglone arrested the cell cycle, induced apoptosis, increased the cleavage of caspase 3
Apoptosis↑,
cl‑Casp3↑,
BAX↑, protein expression of Bax and Cyt c
Cyt‑c↑,
ROS↑, juglone treatment considerably increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels
MDA↑,
GPx4↓, suppressed glutathione peroxidase 4 (GPX4) and superoxide dismutase (SOD) activities
SOD↓,
PI3K↓, inhibited the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway
Akt↓,
eff↓, N-acetylcysteine (a ROS scavenger) partially reversed the positive effects of juglone in terms of migration, invasion, ROS production, apoptosis, and PI3K/Akt pathway-associated protein expression

1925- JG,    Redox regulation of mitochondrial functional activity by quinones
- in-vitro, NA, NA
other↓, Quinones are among the rare compounds successfully used as therapeutic agents to correct mitochondrial diseases and as specific regulators of mitochondrial function within cells.
ROS↑, The stimulation of ROS production by juglone and 2,5-di-tert-butyl-1,4-benzoquinone
MMP↓, dissipation of the mitochondrial membrane potential
eff↝, all the quinones, except for coenzyme Q10, decreased the mitochondrial membrane potential. Juglone, 1,4-benzoquinone, and menadione showed the most pronounced effects.

1926- JG,    Mechanism of juglone-induced apoptosis of MCF-7 cells by the mitochondrial pathway
- in-vitro, BC, MCF-7
TumCG↓, Juglone inhibited the growth of MCF-7 cell line with an IC50 of 11.99 μM.
ROS↑, juglone-exposed cells exhibited significant elevation in intracellular ROS level
MMP↓, decrease in mitochondrial membrane potential
i-Ca+2↑, increase in intracellular Ca(2+) concentration
BAX↑, Juglone upregulated the expression of Bax, and downregulated the expression of Bcl-2, promoting the release of cytochrome C
Bcl-2↓,
Cyt‑c↑,
Casp3?, thereby upregulating the activity of caspase-3

1927- JG,    Juglone-induced apoptosis in human gastric cancer SGC-7901 cells via the mitochondrial pathway
- in-vitro, GC, SGC-7901
Apoptosis↑, rate of apoptosis was found to increase in a dose-dependent manner
ROS↑, juglone at the same dose for 24h, the level of ROS was significantly higher
Bcl-2↓, Bcl-2 was significantly down-regulated and the expression of Bax was significantly up-regulated
BAX↑,
MMP↓, mitochondrial transmembrane potential was significantly lower
Cyt‑c↑, expression of the cytochrome c protein was significantly higher relative to the control
Casp3?, Caspase 3 was activated in a concentration-dependent manner
Bax:Bcl2↑, reduction in the Bcl-2/Bax ratio


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   p‑Akt↓,1,   AMPK↑,1,   Apoptosis↑,5,   BAD↑,1,   BAX↑,4,   Bax:Bcl2↑,1,   Bcl-2↓,3,   Bcl-xL↓,1,   Beclin-1↑,1,   i-Ca+2↑,1,   Casp3?,2,   cl‑Casp3↑,2,   Casp8↑,1,   CDC25↓,1,   CDK1↓,1,   CDK2↓,1,   cycA1↓,1,   Cyt‑c↑,4,   Dose↝,1,   DR5↑,1,   E-cadherin↑,1,   eff↓,4,   eff↝,1,   Ferroptosis↑,1,   FOSL1↑,1,   GPx4↓,1,   GSH↓,1,   GSK‐3β↑,1,   H2O2↑,1,   Hif1a↓,1,   HO-1↑,1,   Iron↑,1,   LC3I↑,1,   LC3II↑,1,   lipid-P↑,1,   MDA↑,2,   MMP↓,3,   MMP9↓,1,   mTOR↑,1,   N-cadherin↓,1,   OS↑,1,   other↓,1,   P21↑,1,   p‑p38↑,1,   P53↑,1,   p62↓,1,   PARP↑,1,   PI3K↓,1,   ROS↑,11,   selectivity↑,1,   Snail↓,1,   SOD↓,1,   toxicity↝,1,   TumAuto↑,2,   TumCCA↑,2,   TumCG↓,3,   TumCI↓,2,   TumCMig↓,2,   TumCP↓,4,   tumCV↓,2,   VEGF↓,1,   Vim↓,1,  
Total Targets: 63

Results for Effect on Normal Cells:

Total Targets: 0

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