cJun Cancer Research Results

cJun, cellular Transcription factor Jun: Click to Expand ⟱
Source:
Type: Oncogene
Transcription factor Jun is a protein that in humans is encoded by the JUN gene.
Increased c-jun gene and c-Jun protein expression, and stimulation of c-Jun phosphorylation has been noted under a variety of conditions. Most important member of the AP-1 transcription factor family.
Scientific Papers found: Click to Expand⟱
5870- CA,    Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen‐Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells
- vitro+vivo, BC, T47D - in-vitro, BC, MCF-7
ROS↑, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
cJun↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
p38↑,
eff↓, The antioxidant N‐acetyl‐L‐cysteine (5 μM) abolished CA‐induced apoptosis.
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓,
Apoptosis↑, CA Induced Breast Cancer Apoptosis
BAX↑, Bax and PARP expression levels increased significantly while Bcl‐2 expression decreased with time
PARP↑,
Bcl-2↓,
TumCG↑, CA Suppressed Growth of Breast Cancer Xenografts in Nude Mice
Ki-67↓, down‐regulating Ki67 and Bcl‐2 in vivo.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,

5874- CA,    Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen-Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells
- vitro+vivo, BC, T47D - in-vitro, BC, MCF10
AntiTum↓, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
ROS↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
cJun↑, CA Activated JNK and p38 in Breast Cancer Cell Lines
p‑p38↑,
Apoptosis↑, CA induced apoptosis of hepatocellular carcinoma cells via the reactive oxygen species (ROS)‐mediated mitochondrial pathway
ROS↑,
eff↑, Furthermore, the combined application of CA and curcumin suppressed the proliferative activity and disrupted the mitochondrial function of metastatic prostate cancer cells compared with their individual uses
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓, Glucose consumption was accelerated by low concentrations of CA, but decreased with increasing time and CA concentration.
BAX↑, up‐regulating Bax and PARP and down‐regulating Bcl‐2.
PARP↑,
Bcl-2↓,
eff↓, We then abrogated the effect of CA‐induced ROS using the antioxidant NAC (5 mM).
Ki-67↓, These findings indicated that CA could accelerate tumor apoptosis by up‐regulating Bax expression and down‐regulating Ki67 and Bcl‐2 in vivo.
toxicity↝, Furthermore, CA did not injure vital organs.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,

2844- FIS,    Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells
- in-vitro, OS, U2OS
tumCV↓, Fisetin at 20-100 µM effectively reduced the viability of OS cells, and induced apoptosis by signifi-cantly inducing the expression of Caspases- 3,-8 and -9 and pro-apoptotic proteins (Bax and Bad) with subsequent down-regulation of Bcl-xL and Bcl-2
Apoptosis↑,
Casp3↑,
Casp8↑,
Casp9↑,
BAX↑,
BAD↑,
Bcl-2↓,
Bcl-xL↓,
PI3K↓, inhibited PI3K/Akt pathway and ERK1/2,
Akt↓,
ERK↓,
p‑JNK↑, it caused enhanced expressions of p-JNK, p-c-Jun and p-p38
p‑cJun↑,
p‑p38↑,
ROS↑, Fisetin-induced ROS generation and decrease in mitochondrial membrane potential
MMP↓, noticeable decline of mitochondrial transmembrane potential (ΔΨm) in a dose-dependent manner
mTORC1↓, fisetin at various concentrations (20-100 μM) caused a significant (p<0.05) decrease in the level of p-Akt and mTORC1 (an important effector protein of Akt), while up-regulated PTEN.
PTEN↑,
p‑GSK‐3β↓, Level of phosphorylated glycogensynthase kinase 3ǃ (GSK3ǃ), (a serine/threonine kinase) and cyclin D1 were potentially decreased by fisetin which is in line with raised non-phosphorylated levels of GSK3ǃ
GSK‐3β↑,
NF-kB↓, Down-regualtion of NF-κB along with significant up-regulations in IκB upon fisetin treatment correlates with the down-regulation of p-Akt levels.
IKKα↑,
Cyt‑c↑, activates the efflux of cytochrome C

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↑, induced ISH and HEC-1B cell cycle arrest at the G1 phase and G2/M phase, respectively
P53↑,
P21↑,
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
CycB/CCNB1↓,
p‑cJun↑,

2864- HNK,    Honokiol: A Review of Its Anticancer Potential and Mechanisms
- Review, Var, NA
TumCCA↑, induction of G0/G1 and G2/M cell cycle arrest
CDK2↓, (via the regulation of cyclin-dependent kinase (CDK) and cyclin proteins),
EMT↓, epithelial–mesenchymal transition inhibition via the downregulation of mesenchymal markers
MMPs↓, honokiol possesses the capability to supress cell migration and invasion via the downregulation of several matrix-metalloproteinases
AMPK↑, (activation of 5′ AMP-activated protein kinase (AMPK) and KISS1/KISS1R signalling)
TumCI↓, inhibiting cell migration, invasion, and metastasis, as well as inducing anti-angiogenesis activity (via the down-regulation of vascular endothelial growth factor (VEGFR) and vascular endothelial growth factor (VEGF)
TumCMig↓,
TumMeta↓,
VEGFR2↓,
*antiOx↑, diverse biological activities, including anti-arrhythmic, anti-inflammatory, anti-oxidative, anti-depressant, anti-thrombocytic, and anxiolytic activities
*Inflam↓,
*BBB↑, Due to its ability to cross the blood–brain barrier
*neuroP↑, beneficial towards neuronal protection through various mechanism, such as the preservation of Na+/K+ ATPase, phosphorylation of pro-survival factors, preservation of mitochondria, prevention of glucose, reactive oxgen species (ROS), and inflammatory
*ROS↓,
Dose↝, Generally, the concentrations used for the in vitro studies are between 0–150 μM
selectivity↑, Interestingly, honokiol has been shown to exhibit minimal cytotoxicity against on normal cell lines, including human fibroblast FB-1, FB-2, Hs68, and NIH-3T3 cells
Casp3↑, ↑ Caspase-3 & caspase-9
Casp9↑,
NOTCH1↓, Inhibition of Notch signalling: ↓ Notch1 & Jagged-1;
cycD1/CCND1↓, ↓ cyclin D1 & c-Myc;
cMyc↓,
P21?, ↑ p21WAF1 protein
DR5↑, ↑ DR5 & cleaved PARP
cl‑PARP↑,
P53↑, ↑ phosphorylated p53 & p53
Mcl-1↑, ↓ Mcl-1 protein
p65↓, ↓ p65; ↓ NF-κB
NF-kB↓,
ROS↑, ↑ JNK activation ,Increase ROS activity:
JNK↑,
NRF2↑, ↑ Nrf2 & c-Jun protein activation
cJun↑,
EF-1α↓, ↓ EFGR; ↓ MAPK/PI3K pathway activity
MAPK↓,
PI3K↓,
mTORC1↓, ↓ mTORC1 function; ↑ LKB1 & cytosolic localisation
CSCs↓, Inhibit stem-like characteristics: ↓ Oct4, Nanog & Sox4 protein; ↓ STAT3;
OCT4↓,
Nanog↓,
SOX4↓,
STAT3↓,
CDK4↓, ↓ Cdk2, Cdk4 & p-pRbSer780;
p‑RB1↓,
PGE2↓, ↓ PGE2 production ↓ COX-2 ↑ β-catenin
COX2↓,
β-catenin/ZEB1↑,
IKKα↓, ↓ IKKα
HDAC↓, ↓ class I HDAC proteins; ↓ HDAC activity;
HATs↑, ↑ histone acetyltransferase (HAT) activity; ↑ histone H3 & H4
H3↑,
H4↑,
LC3II↑, ↑ LC3-II
c-Raf↓, ↓ c-RAF
SIRT3↑, ↑ Sirt3 mRNA & protein; ↓ Hif-1α protein
Hif1a↓,
ER Stress↑, ↑ ER stress signalling pathway activation; ↑ GRP78,
GRP78/BiP↑,
cl‑CHOP↑, ↑ cleaved caspase-9 & CHOP;
MMP↓, mitochondrial depolarization
PCNA↓, ↓ cyclin B1, cyclin D1, cyclin D2 & PCNA;
Zeb1↓, ↓ ZEB2 Inhibit
NOTCH3↓, ↓ Notch3/Hes1 pathway
CD133↓, ↓ CD133 & Nestin protein
Nestin↓,
ATG5↑, ↑ Atg7 protein activation; ↑ Atg5;
ATG7↑,
survivin↓, ↓ Mcl-1 & survivin protein
ChemoSen↑, honokiol potentiated the apoptotic effect of both doxorubicin and paclitaxel against human liver cancer HepG2 cells.
SOX2↓, Honokiol was shown to downregulate the expression of Oct4, Nanog, and Sox2 which were known to be expressed in osteosarcoma, breast carcinoma and germ cell tumours
OS↑, Lipo-HNK was also shown to prolong survival and induce intra-tumoral apoptosis in vivo.
P-gp↓, Honokiol was shown to downregulate the expression of P-gp at mRNA and protein levels in MCF-7/ADR, a human breast MDR cancer cell line
Half-Life↓, For i.v. administration, it has been found that there was a rapid rate of distribution followed by a slower rate of elimination (elimination half-life t1/2 = 49.22 min and 56.2 min for 5 mg or 10 mg of honokiol, respectively
Half-Life↝, male and female dogs was assessed. The elimination half-life (t1/2 in hours) was found to be 20.13 (female), 9.27 (female), 7.06 (male), 4.70 (male), and 1.89 (male) after administration of doses of 8.8, 19.8, 3.9, 44.4, and 66.7 mg/kg, respectively.
eff↑, Apart from that, epigallocatechin-3-gallate functionalized chitin loaded with honokiol nanoparticles (CE-HK NP), developed by Tang et al. [224], inhibit HepG2
BioAv↓, extensive biotransformation of honokiol may contribute to its low bioavailability.

67- QC,  RES,    Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
cJun↑, Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
AR↓,

2085- TQ,    Anticancer Activities of Nigella Sativa (Black Cumin)
- Review, Var, NA
MMP↓, TQ induces apoptosis, disrupts mitochondrial membrane potential and triggers the activation of caspases 8, 9 and 3 in HL-60 cells.
Casp3↑,
Casp8↑,
Casp9↓,
cl‑PARP↑, PARP cleavage and the release of cytochrome c from mitochondria into the cytoplasm.
Cyt‑c↑,
Bax:Bcl2↑, marked increase in Bax/Bcl2 ratios
NF-kB↓, TQ also down-regulates the expression of NF-kappa B-regulated antiapoptotic (IAP1, IAP2, XIAP Bcl-2, Bcl-xL, and survivin) gene products
IAP1↓,
IAP2↓,
XIAP↓,
Bcl-xL↓,
survivin↓,
cJun↑, TQ inducing apoptosis by the activation of c-Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase pathways in pancreatic cancer cell.
p38↑,
Akt↑, TQ effectively inhibited human umbilical vein endothelial cell migration, invasion, and tube formation by suppressing the activation of AKT
chemoP↑, TQ can lower the toxicity of other anticancer drugs (for example, cyclophosphamide) by an up-regulation of antioxidant mechanisms, indicating a potential clinical application for these agents to minimize the toxic effects of treatment with anticancer
*radioP↑, Cemek et al. (2006) showed that N. sativa and glutathione treatment significantly antagonize the effects of radiation. Therefore, N. sativa may be a beneficial agent in protection against ionizing radiation-related tissue injury.

2102- TQ,    A review on therapeutic potential of Nigella sativa: A miracle herb
- Review, Var, NA
angioG↓, TQ inhibits tumor angiogenesis and tumor growth through suppressing NF-κB and its regulated molecules.
NF-kB↓,
PPARγ↓, TQ was found to increase PPAR-γ activity and down-regulate the expression of the genes for Bcl-2, Bcl-xL and survivin in breast cancer cells.
Bcl-2↓,
Bcl-xL↓,
MUC4↓, TQ down regulated MUC4 expression through the proteasomal pathway and induced apoptosis in pancreatic cancer cells by the activation of c-Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase pathways
cJun↑,
p38↑,
P21↑, TQ also increased p21 WAF1 expression, inhibited HDAC activity, and induced histone hyperacetylation
HDAC↓,
*radioP↑, N. sativa oil is a promising natural radioprotective agent against immunosuppressive and oxidative effects of ionizing radiation
hepatoP↑, Results suggested that N. sativa treatment protects the rat liver against hepatic ischemia reperfusion injury

1817- VitK2,    Research progress on the anticancer effects of vitamin K2
- Review, Var, NA
TumCCA↑, involving cell-cycle arrest
Apoptosis↑, apoptosis, autophagy and invasion
TumAuto↑,
TumCI↓,
TumCG↓, inhibit the growth of cancer cells
ChemoSen↓, combination treatment of VK2 and established chemotherapeutics may achieve better results, with fewer side effects
ChemoSideEff↓,
toxicity∅, VK2 is milder, but causes no side effects, whereas VK1 has the least strong function
eff↑, combination of VK2 and vitamin E suppressed the growth of the primary tumor and obliterated the intraperitoneal dissemination in a 65-year-old man with ruptured HCC
cycD1/CCND1↓, decreases in cyclin D1 and cyclin-dependent kinase 4 (CDK4) levels
CDK4↓,
eff↑, pretreatment with VK2 prior to sorafenib treatment is proven to exert more effective HCC growth inhibition in animals than treatment with either alone
IKKα↓, VK2 can inhibit the IκB kinase (IKK)/IκB/NF-κB pathway
NF-kB↓,
other↑, stimulate the phosphorylation of PKA and activate activating protein 2 (AP-2)
p27↑, VK2 upregulates the expression of p27
cMyc↓, 5 µΜ VK2 exposure inhibited c-MYC expression in HL-60 leukemia cells
i-ROS↑, VK2 treatment increased the intracellular level of the reactive oxygen species (ROS)
Bcl-2↓, VK2 decreases Bcl-2 expression and increases the expression of Bcl-2-associated X protein (Bax)
BAX↑,
p38↑, VK2 activates p38 MAPK to its phosphorylated form
MMP↓, mitochondrial membrane potential was depolarized and caspase-9 was activated
Casp9↑,
p‑ERK↓, VK2 is reported to inhibit ERK phosphorylation by suppressing Ras activation
RAS↓,
MAPK↓, subsequently suppressing the activation of MAPK kinase (MEK)
p‑P53↑, VK2 stimulated the extrinsic apoptosis pathway by increasing p53 phosphorylation
Casp8↑, caspase-8 activation and further activates caspase-3
Casp3↑,
cJun↑, increasing the expression of c-JUN and c-MYC;
MMPs↓, downregulating the expression of matrix metalloproteinases (MMPs)
eff↑, combination of VK2 with other chemotherapy agents can produce stronger effects than the use of either alone
eff↑, combination of vitamin D3 with VK2 on cancer cells can synergistically improve the induction of cellular differentiation and also significantly reduces the risk of hypercalcemia and vascular calcification

1832- VitK3,  VitC,    Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism
- in-vitro, AML, K562
ROS↑, vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress
H2O2↑, hydrogen peroxide generation,
NF-kB↑, activation of NF-κB,
P53↑, p53, c-Jun, protease caspase-3 activation
cJun↑,
Casp3↑,
MMP↓, mitochondria depolarization leading to nuclei fragmentation
DNAdam↑,
Dose?, Jurkat and K562 cells are exposed to VC and VK3 in a ratio 1000:1 (10 mM: 10 μM) or 100:1 (300 μM: 3 μM), respectively


Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   NRF2↑, 1,   ROS↑, 6,   i-ROS↑, 1,   SIRT3↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 5,   c-Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 2,   glucose↓, 2,   PPARγ↓, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   Apoptosis↑, 4,   BAD↑, 1,   BAX↑, 4,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Bcl-xL↓, 3,   Casp3↑, 5,   Casp8↑, 3,   Casp9↓, 1,   Casp9↑, 3,   Cyt‑c↑, 2,   DR5↑, 1,   IAP1↓, 1,   IAP2↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↓, 2,   Mcl-1↑, 1,   p27↑, 1,   p38↑, 4,   p‑p38↑, 2,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

EF-1α↓, 1,  

Transcription & Epigenetics ⓘ

cJun↑, 8,   p‑cJun↑, 2,   H3↑, 1,   H4↑, 1,   HATs↑, 1,   other↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

cl‑CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 3,   p‑P53↑, 1,   PARP↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 2,   CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   P21?, 1,   P21↑, 2,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CSCs↓, 1,   EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 2,   mTOR↓, 2,   mTORC1↓, 2,   Nanog↓, 1,   Nestin↓, 1,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 4,   PTEN↑, 1,   RAS↓, 1,   SOX2↓, 1,   STAT3↓, 3,   TumCG↓, 1,   TumCG↑, 1,  

Migration ⓘ

Ki-67↓, 2,   MMPs↓, 2,   MUC4↓, 1,   SOX4↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IKKα↓, 2,   IKKα↑, 1,   NF-kB↓, 5,   NF-kB↑, 1,   p65↓, 1,   PGE2↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↓, 1,   ChemoSen↑, 1,   Dose?, 1,   Dose↝, 1,   eff↓, 2,   eff↑, 6,   Half-Life↓, 1,   Half-Life↝, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   Ki-67↓, 2,  

Functional Outcomes ⓘ

AntiTum↓, 1,   chemoP↑, 1,   ChemoSideEff↓, 1,   hepatoP↑, 1,   OS↑, 1,   toxicity↝, 1,   toxicity∅, 1,  
Total Targets: 128

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,   radioP↑, 2,  
Total Targets: 6

Scientific Paper Hit Count for: cJun, cellular Transcription factor Jun
2 Carnosic acid
2 Thymoquinone
1 Fisetin
1 Garcinol
1 Honokiol
1 Quercetin
1 Resveratrol
1 Vitamin K2
1 VitK3,menadione
1 Vitamin C (Ascorbic Acid)
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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