JNK Cancer Research Results

JNK, c-Jun N-terminal kinase (JNK): Click to Expand ⟱
Source:
Type:
JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. Janus signaling promotes cancer cell survival.
JNK, or c-Jun N-terminal kinase, is a member of the mitogen-activated protein kinase (MAPK) family. It plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). JNK is activated in response to various stress signals, such as UV radiation, oxidative stress, and inflammatory cytokines.
JNK activation can promote apoptosis in cancer cells, acting as a tumor suppressor. However, in other contexts, it can promote cell survival and proliferation, contributing to tumor progression.

JNK is often unregulated in cancers, leading to increased cancer cell proliferation, survival, and resistance to apoptosis. This activation is typically associated with poor prognosis and aggressive tumor behavior.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
5444- AG,    A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine
- Review, Var, NA
*Imm↑, *antiOx↑, *Inflam↓, AntiTum↑, eff↑, chemoP↑, Dose↝, TumCMig↓, TumCP↓, Akt↓, GSK‐3β↓, MMP2↓, MMP9↓, EMT↓, PI3K↓, Akt↓, NF-kB↓, Inflam↓, TGF-β1↓, TNF-α↓, IL6↓, Fas↓, FasL↓, NOTCH1↓, JNK↓, TumCG↓,
5431- AG,    Advances in research on the anti-tumor mechanism of Astragalus polysaccharides
- Review, Var, NA
AntiTum↑, TumCG↓, TumCI↓, Apoptosis↑, Imm↑, Bcl-2↓, BAX↑, Wnt↓, β-catenin/ZEB1↓, TumCG↓, miR-133a-3p↑, JNK↓, Fas↑, P53↑, P21↑, NOTCH1↓, NOTCH3↓, TumCP↓, TumCCA↑, GPx4↓, xCT↓, AMPK↑, Beclin-1↑, NF-kB↓, EMT↓, Vim↓, TumMeta↓, VEGF↓, EGFR↓, eff↑, eff↑, MMP↓, P-gp↓, MMP9↓, ChemoSen↑, SIRT1↓, SREBP1↓, TumAuto↑, PI3K↓, mTOR↓, Casp3↑, Casp9↑, CD133↓, CD44↓, CSCs↓, QoL↑,
2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, ITGB4↓, TumCI↓, TumMeta↓, Akt↓, ERK↓, p‑JNK↓, *Inflam↓, *PKCδ↓, *MAPK↓, EGFR↓, CK2↓, TumCCA↑, CDK1↓, P53↓, P21↑, Bax:Bcl2↑, Cyt‑c↑, APAF1↑, Casp↑, cl‑PARP↑, VEGF↓, Hif1a↓, IGF-1↓, IGFBP3↑, E-cadherin↑, β-catenin/ZEB1↓, HSPs↓, Telomerase↓, FASN↓, MMPs↓, HER2/EBBR2↓, CK2↓, eff↑, AntiAg↑, eff↑, FAK↓, ROS↑, Bcl-2↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp7↑, cl‑Casp8↑, cl‑Casp9↑, cl‑IAP2↑, AR↓, PSA↓, p‑pRB↓, p‑GSK‐3β↓, CDK4↓, ChemoSen↑, Ca+2↑, cal2↑,
3391- ART/DHA,    Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug
- Review, Var, NA
TumCP↓, TumMeta↓, angioG↓, TumVol↓, BioAv↓, Half-Life↓, BioAv↑, eff↑, eff↓, ROS↑, selectivity↑, TumCCA↑, survivin↓, BAX↑, Casp3↓, Casp8↑, Casp9↑, CDC25↓, CycB/CCNB1↓, NF-kB↓, cycD1/CCND1↓, cycE/CCNE↓, E2Fs↓, P21↑, p27↑, ADP:ATP↑, MDM2↓, VEGF↓, IL8↓, COX2↓, MMP9↓, ER Stress↓, cMyc↓, GRP78/BiP↑, DNAdam↑, AP-1↓, MMP2↓, PKCδ↓, Raf↓, ERK↓, JNK↓, PCNA↓, CDK2↓, CDK4↓, TOP2↓, uPA↓, MMP7↓, TIMP2↑, Cdc42↑, E-cadherin↑,
2735- BetA,    Betulinic acid as apoptosis activator: Molecular mechanisms, mathematical modeling and chemical modifications
- Review, Var, NA
mt-Apoptosis↑, Casp↑, p38↑, MAPK↓, JNK↓, VEGF↓, AIF↑, Cyt‑c↑, ROS↑, Ca+2↑, ATP↓, NF-kB↓, ATF3↓, TOP1↓, VEGF↓, survivin↓, Sp1/3/4↓, MMP↓, ChemoSen↑, selectivity↑, BioAv↓, BioAv↑, BioAv↑, BioAv↑, BioAv↑,
5680- BML,    Anticancer properties of bromelain: State-of-the-art and recent trends
- Review, Var, NA
*Inflam↓, *Bacteria↓, *Pain↓, *Diar↓, *Wound Healing↑, ERK↓, JNK↓, XIAP↓, HSP27↓, β-catenin/ZEB1↓, HO-1↓, lipid-P↓, ACSL4↑, ROS↑, SOD↑, Catalase↓, GSH↓, MDA↓, Casp3↓, Casp9↑, DNAdam↑, Apoptosis↑, NF-kB↓, P53↑, MAPK↓, APAF1↑, Cyt‑c↓, CD44↓, Imm↑, ATG5↑, LC3I↑, Beclin-1↑, IL2↓, IL4↓, IFN-γ↓, COX2↓, iNOS↓, ChemoSen↑, RadioS↑, Dose↝, other↓,
2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, *TNF-α↓, *MMP3↓, *COX1↓, *COX2↓, *PGE2↓, *Th2↑, *Catalase↑, *SOD↑, *NO↑, *PGE2↑, *IL1β↓, *IL6↓, *Th1 response↓, *Th2↑, *iNOS↓, *NO↓, *p‑JNK↓, *p38↓, GutMicro↑, p‑Akt↓, GSK‐3β↓, cycD1/CCND1↓, Akt↓, STAT3↓, CSCs↓, AR↓, P21↑, DR5↑, CHOP↑, Casp3↑, Casp8↑, cl‑PARP↑, DNAdam↑, p‑RB1↓, FOXM1↓, TOP2↓, CDC25↓, p‑CDK1↓, p‑ERK↓, MMP9↓, VEGF↓, angioG↓, ROS↑, Cyt‑c↑, AIF↑, Diablo↑, survivin↓, ICAD↓, ChemoSen↑, SOX9↓, ER Stress↑, GRP78/BiP↑, cal2↓, AMPK↓, mTOR↓, ROS↓,
6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,
3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, DNMTs↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, HATs↓, HDAC↓, selectivity↑, uPA↓, NF-kB↓, TNF-α↓, *ROS↓, *antiOx↑, Hif1a↓, VEGF↓, MMP2↓, MMP9↓, FAK↓, TIMP2↑, Mcl-1↓, survivin↓, XIAP↓, PCNA↓, p16↑, P21↑, p27↑, pRB↑, P53↑, MDM2↑, ROS↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Diablo↑, BAX⇅, cl‑PPARα↓, PDGF↓, EGFR↓, FOXO↑, AP-1↓, JNK↓, COX2↓, angioG↓,
1661- PBG,    Propolis: a natural compound with potential as an adjuvant in cancer therapy - a review of signaling pathways
- Review, Var, NA
JNK↓, ERK↓, Akt↓, NF-kB↓, FAK↓, MAPK↓, PI3K↓, Akt↓, P21↑, p27↑, TRAIL↑, BAX↑, P53↑, ERK↓, ChemoSen↑, RadioS↑, Glycolysis↓, HK2↓, PKM2↓, LDHA↓, PFK↓,
3249- PBG,    Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence
- Review, Var, NA
*Inflam↓, *ROS↓, *MDA↓, *TNF-α↓, *NO↓, *iNOS↓, *SOD↑, *GPx↑, *GSR↓, *GSH↑, *neuroP↑, *IL6↓, *MMP2↓, *MMP9↓, *MCP1↓, *HSP70/HSPA5↑, *motorD↑, *Pain↓, *VCAM-1↓, *NF-kB↓, *MAPK↓, *JNK↓, *IL1β↓, *AChE↓, *toxicity∅, cognitive↑,
4918- PEITC,    Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic Insights
- Review, Var, NA
Apoptosis↑, TumCP↓, angioG↓, TumMeta↓, NF-kB↓, Akt↓, MAPK↓, *BioAv↓, ROS↑, lipid-P↑, AIF↑, Cyt‑c↑, DR4↑, DR5↑, TumCCA↑, JAK↓, STAT3↓, MMP2↓, MMP9↓, PKCδ↓, Hif1a↓, JNK↓, Mcl-1↓, COX2↓, MMP↓, Casp3↑, ChemoSen↑, *BioAv↓, Half-Life↓,
3079- RES,    Therapeutic role of resveratrol against hepatocellular carcinoma: A review on its molecular mechanisms of action
- Review, Var, NA
angioG↓, TumMeta↓, ChemoSen↑, NADPH↑, SIRT1↑, NF-kB↓, NLRP3↓, Dose↝, COX2↓, MMP9↓, PGE2↓, TIMP1↑, TIMP2↑, Sp1/3/4↓, p‑JNK↓, uPAR↓, ROS↓, CXCR4↓, IL6↓, Gli1↓, *ROS↓, *GSTs↑, *SOD↑, *Catalase↑, *GPx↑, *lipid-P↓, *GSH↑, eff↑, eff↑, eff↑,
1744- RosA,    Therapeutic Applications of Rosmarinic Acid in Cancer-Chemotherapy-Associated Resistance and Toxicity
- Review, Var, NA
chemoR↓, ChemoSideEff↓, RadioS↑, ROS↓, ChemoSen↑, BioAv↑, Half-Life↝, antiOx↑, ROS↑, Fenton↑, DNAdam↑, Apoptosis↑, CSCs↓, HH↓, Bax:Bcl2↑, MDR1↓, P-gp↓, eff↑, eff↑, FOXO4↑, *eff↑, *ROS↓, *JNK↓, *ERK↓, *GSH↑, *H2O2↑, *MDA↓, *SOD↑, *HO-1↑, *CardioT↓, selectivity↑,
3001- RosA,    Therapeutic Potential of Rosmarinic Acid: A Comprehensive Review
- Review, Var, NA
TumCP↓, Apoptosis↑, TumMeta↓, Inflam↓, *antiOx↑, *AntiAge↑, *ROS↓, BioAv↑, Dose↝, NRF2↑, P-gp↑, ATP↑, MMPs↓, cl‑PARP↓, Hif1a↓, GlucoseCon↓, lactateProd↓, Warburg↓, TNF-α↓, COX2↓, IL6↓, HDAC2↓, GSH↑, ROS↓, ChemoSen↑, *BG↓, *IL1β↓, *TNF-α↓, *IL6↓, *p‑JNK↓, *p38↓, *Catalase↑, *SOD↑, *GSTs↑, *VitC↑, *VitE↑, *GSH↑, *GutMicro↑, *cardioP↑, *ROS↓, *MMP↓, *lipid-P↓, *NRF2↑, *hepatoP↑, *neuroP↑, *P450↑, *HO-1↑, *AntiAge↑, *motorD↓,
3301- SIL,    Critical review of therapeutic potential of silymarin in cancer: A bioactive polyphenolic flavonoid
- Review, Var, NA
Inflam↓, TumCCA↑, Apoptosis↓, TumMeta↓, TumCG↓, angioG↓, chemoP↑, radioP↑, p‑ERK↓, p‑p38↓, p‑JNK↓, P53↑, Bcl-2↓, Bcl-xL↓, TGF-β↓, MMP2↓, MMP9↓, E-cadherin↑, Wnt↓, Vim↓, VEGF↓, IL6↓, STAT3↓, *ROS↓, IL1β↓, PGE2↓, CDK1↓, CycB/CCNB1↓, survivin↓, Mcl-1↓, Casp3↑, Casp9↑, cMyc↓, COX2↓, Hif1a↓, CXCR4↓, CSCs↓, EMT↓, N-cadherin↓, PCNA↓, cycD1/CCND1↓, ROS↑, eff↑, eff↑, eff↑, HER2/EBBR2↓,

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ATF3↓, 1,   Catalase↓, 1,   Fenton↑, 1,   GPx4↓, 1,   GSH↓, 1,   GSH↑, 1,   HO-1↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   lipid-P↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 4,   ROS↑, 10,   SOD↑, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 1,   AIF↑, 3,   ATP↓, 1,   ATP↑, 1,   CDC25↓, 2,   mitResp↓, 1,   MMP↓, 3,   mtDam↑, 1,   Raf↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↓, 1,   AMPK↑, 1,   cMyc↓, 3,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   NADPH↑, 1,   PFK↓, 1,   PKM2↓, 1,   cl‑PPARα↓, 1,   SIRT1↓, 1,   SIRT1↑, 1,   SREBP1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 8,   p‑Akt↓, 1,   APAF1↑, 2,   Apoptosis↓, 1,   Apoptosis↑, 5,   mt-Apoptosis↑, 1,   BAX↑, 3,   BAX⇅, 1,   Bax:Bcl2↑, 3,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp↑, 2,   Casp3↓, 2,   Casp3↑, 6,   cl‑Casp3↑, 1,   cl‑Casp7↑, 1,   Casp8↑, 3,   cl‑Casp8↑, 1,   Casp9↑, 6,   cl‑Casp9↑, 1,   CK2↓, 2,   Cyt‑c↓, 1,   Cyt‑c↑, 6,   Diablo↑, 2,   DR4↑, 1,   DR5↑, 2,   Fas↓, 1,   Fas↑, 1,   FasL↓, 1,   cl‑IAP2↑, 1,   ICAD↓, 1,   iNOS↓, 1,   JNK↓, 8,   p‑JNK↓, 3,   MAPK↓, 4,   Mcl-1↓, 3,   MDM2↓, 1,   MDM2↑, 1,   p27↑, 3,   p38↑, 1,   p‑p38↓, 1,   survivin↓, 5,   Telomerase↓, 2,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,   SOX9↓, 1,   Sp1/3/4↓, 2,  

Transcription & Epigenetics ⓘ

HATs↓, 1,   other↓, 1,   pRB↑, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↓, 1,   ER Stress↑, 1,   GRP78/BiP↑, 2,   HSP27↓, 1,   HSPs↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 2,   LC3I↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 4,   DNMTs↓, 1,   p16↑, 1,   P53↓, 1,   P53↑, 5,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↓, 1,   cl‑PARP↑, 2,   PCNA↓, 4,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   p‑CDK1↓, 1,   CDK2↓, 3,   CDK4↓, 3,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 5,   cycE/CCNE↓, 2,   E2Fs↓, 1,   P21↑, 6,   p‑RB1↓, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 2,   CSCs↓, 4,   EMT↓, 3,   EMT↝, 1,   ERK↓, 5,   p‑ERK↓, 2,   FOXM1↓, 1,   FOXO↑, 1,   FOXO4↑, 1,   Gli1↓, 1,   GSK‐3β↓, 2,   p‑GSK‐3β↓, 2,   HDAC↓, 1,   HDAC2↓, 1,   HH↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   mTOR↓, 3,   NOTCH1↓, 2,   NOTCH3↓, 1,   PI3K↓, 4,   STAT3↓, 3,   TOP1↓, 1,   TOP2↓, 2,   TumCG↓, 5,   Wnt↓, 2,  

Migration ⓘ

AntiAg↑, 1,   AP-1↓, 2,   Ca+2↑, 2,   cal2↓, 1,   cal2↑, 1,   Cdc42↑, 1,   E-cadherin↑, 4,   FAK↓, 3,   ITGB4↓, 1,   miR-133a-3p↑, 1,   MMP2↓, 5,   MMP7↓, 1,   MMP9↓, 8,   MMPs↓, 2,   N-cadherin↓, 2,   PDGF↓, 1,   PKCδ↓, 2,   TGF-β↓, 1,   TGF-β1↓, 1,   TIMP1↑, 1,   TIMP2↑, 3,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 5,   TumMeta↓, 7,   uPA↓, 2,   uPAR↓, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,   EGFR↓, 3,   Hif1a↓, 6,   VEGF↓, 9,  

Barriers & Transport ⓘ

P-gp↓, 2,   P-gp↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 7,   CXCR4↓, 2,   IFN-γ↓, 1,   IL1β↓, 1,   IL2↓, 1,   IL4↓, 1,   IL6↓, 4,   IL8↓, 1,   Imm↑, 2,   Inflam↓, 3,   JAK↓, 1,   NF-kB↓, 9,   PGE2↓, 2,   PSA↓, 1,   TNF-α↓, 3,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 7,   chemoR↓, 1,   ChemoSen↑, 11,   Dose↝, 4,   eff↓, 1,   eff↑, 14,   Half-Life↓, 2,   Half-Life↝, 1,   MDR1↓, 1,   RadioS↑, 3,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

AR↓, 2,   EGFR↓, 3,   FOXM1↓, 1,   GutMicro↑, 1,   HER2/EBBR2↓, 2,   IL6↓, 4,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 2,   chemoP↑, 2,   chemoPv↑, 1,   ChemoSideEff↓, 1,   cognitive↑, 1,   OS↑, 1,   QoL↑, 1,   radioP↑, 1,   TumVol↓, 1,  
Total Targets: 235

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 4,   GPx↑, 3,   GSH↑, 5,   GSR↓, 1,   GSTs↑, 2,   H2O2↑, 1,   HO-1↑, 3,   lipid-P↓, 2,   MDA↓, 3,   NRF2↑, 3,   ROS↓, 8,   SOD↑, 6,   VitC↑, 1,   VitE↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   glucose↓, 1,   LDH↓, 1,   PPARα↝, 1,  

Cell Death ⓘ

Casp↓, 1,   iNOS↓, 2,   JNK↓, 3,   p‑JNK↓, 2,   MAPK↓, 2,   p38↓, 2,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   TRPC1↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   NO↓, 2,   NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 2,   IL1β↓, 3,   IL6↓, 4,   Imm↑, 1,   Inflam↓, 5,   MCP1↓, 1,   NF-kB↓, 3,   PGE2↓, 1,   PGE2↑, 1,   Th1 response↓, 1,   Th2↑, 2,   TLR4↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   eff↑, 2,   P450↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   BP↓, 1,   GutMicro↑, 1,   IL6↓, 4,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 2,   CardioT↓, 1,   hepatoP↑, 2,   memory↑, 1,   motorD↓, 1,   motorD↑, 1,   neuroP↑, 4,   Pain↓, 2,   toxicity∅, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Diar↓, 1,  
Total Targets: 77

Scientific Paper Hit Count for: JNK, c-Jun N-terminal kinase (JNK)
2 Astragalus
2 Propolis -bee glue
2 Rosmarinic acid
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Betulinic acid
1 Bromelain
1 Boswellia (frankincense)
1 Chlorogenic acid
1 EGCG (Epigallocatechin Gallate)
1 Phenethyl isothiocyanate
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
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:26  Cells:%  prod#:%  Target#:168  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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