MAPK Cancer Research Results

MAPK, mitogen-activated protein kinase: Click to Expand ⟱
Source: CGL-CS
Type:
Mitogen-activated protein kinases (MAPKs) are a group of proteins involved in transmitting signals from the cell surface to the nucleus, playing a crucial role in various cellular processes, including growth, differentiation, and apoptosis (programmed cell death).

MAPK Pathways: The MAPK family includes several pathways, the most notable being:
1.ERK (Extracellular signal-Regulated Kinase): Often associated with cell proliferation and survival.
2.JNK (c-Jun N-terminal Kinase): Typically involved in stress responses and apoptosis.
3.p38 MAPK: Associated with inflammatory responses and apoptosis.

Inhibitors: Targeting the MAPK pathway has become a strategy in cancer therapy. For example, BRAF inhibitors (like vemurafenib) are used in treating melanoma with BRAF mutations.
Altered Expression Levels:
Overexpression: Many cancers exhibit overexpression of MAPK pathway components, such as RAS, BRAF, and MEK. This overexpression can lead to increased signaling activity, promoting cell proliferation and survival.
Downregulation: In some cases, negative regulators of the MAPK pathway (e.g., MAPK phosphatases) may be downregulated, leading to enhanced MAPK signaling.
The expression levels of MAPK pathway components can serve as biomarkers for cancer diagnosis, prognosis, and treatment response. For example, high levels of phosphorylated ERK (p-ERK) may indicate active MAPK signaling and poor prognosis in certain cancers.

Numerous reports indicate that the MAPK pathway plays a major role in tumor progression and invasion, while inhibition of MAPK signaling reduces invasion.
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⟱
2658- AL,    The Toxic Effect Ways of Allicin on Different Cell Lines
- Review, Var, NA
*antiOx↑, *AntiAg↑, *cardioP↑, Ca+2↑, ROS↑, Casp↑, p38↑, MAPK↑, hepatoP↑, chemoP↑,
2666- AL,    Targeting the Interplay of Autophagy and ROS for Cancer Therapy: An Updated Overview on Phytochemicals
- Review, Var, NA
Inflam↓, AntiCan↑, ROS↑, MAPK↑, JNK↑, TumAuto↑, other↑, Dose↝, MALAT1↓, Wnt↓, β-catenin/ZEB1↓,
3156- Ash,    Withaferin A: From ayurvedic folk medicine to preclinical anti-cancer drug
- Review, Var, NA
MAPK↑, p38↑, BAX↑, BIM↑, CHOP↑, ROS↑, DR5↑, Apoptosis↑, Ferroptosis↑, GPx4↓, BioAv↝, HSP90↓, RET↓, E6↓, E7↓, Akt↓, cMET↓, Glycolysis↓, TCA↓, NOTCH1↓, STAT3↓, AP-1↓, PI3K↓, eIF2α↓, HO-1↑, TumCCA↑, CDK1↓, *hepatoP↑, *GSH↑, *NRF2↑, Wnt↓, EMT↓, uPA↓, CSCs↓, Nanog↓, SOX2↓, CD44↓, lactateProd↓, Iron↑, NF-kB↓,
3160- Ash,    Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal
- Review, Var, NA
TumCCA↑, H3↑, P21↑, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, CDC2↓, CHK1↓, Chk2↓, p38↑, MAPK↑, E6↓, E7↓, P53↑, Akt↓, FOXO3↑, ROS↑, γH2AX↑, MMP↓, mitResp↓, eff↑, TumCD↑, Mcl-1↓, ER Stress↑, ATF4↑, ATF3↑, CHOP↑, NOTCH↓, NF-kB↓, Bcl-2↓, STAT3↓, CDK1↓, β-catenin/ZEB1↓, N-cadherin↓, EMT↓, Cyt‑c↑, eff↑, CDK4↓, p‑RB1↓, PARP↑, cl‑Casp3↑, cl‑Casp9↑, NRF2↑, ER-α36↓, LDHA↓, lipid-P↑, AP-1↓, COX2↓, RenoP↑, PDGFR-BB↓, SIRT3↑, MMP2↓, MMP9↓, NADPH↑, NQO1↑, GSR↑, HO-1↑, *SOD2↑, *Prx↑, *Casp3?, eff↑, Snail↓, Slug↓, Vim↓, CSCs↓, HEY1↓, MMPs↓, VEGF↓, uPA↓, *toxicity↓, CDK2↓, CDK4↓, HSP90↓,
2743- BetA,    Betulinic acid and the pharmacological effects of tumor suppression
- Review, Var, NA
ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, TumCCA↑, Sp1/3/4↓, STAT3↓, NF-kB↓, EMT↓, TOP1↓, MAPK↑, p38↑, JNK↑, Casp↑, Bcl-2↓, BAX↑, VEGF↓, LAMs↓,
2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, AntiCan↑, *MAPK↑, *Ca+2↝, p‑ERK↓, TumCI↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, p‑RB1↓, *NF-kB↓, *TNF-α↓, NF-kB↓, IKKα↓, MCP1↓, IL1α↓, MIP2↓, VEGF↓, Tf↓, COX2↓, MMP9↓, CXCR4↓, VEGF↓, eff↑, PPARα↓, lipid-P?, STAT3↓, TOP1↓, TOP2↑, 5HT↓, p‑PDGFR-BB↓, PDGF↓, AR↓, DR5↑, angioG↓, DR4↑, Casp3↑, Casp8↑, cl‑PARP↑, eff↑, chemoPv↑, Wnt↓, β-catenin/ZEB1↓, ascitic↓, Let-7↑, miR-200b↑, eff↑, MMP1↓, MMP2↓, eff↑, BioAv↓, BioAv↑, Half-Life↓, toxicity↓, Dose↑, BioAv↑, ChemoSen↑,
1651- CA,  PBG,    Caffeic acid and its derivatives as potential modulators of oncogenic molecular pathways: New hope in the fight against cancer
- Review, Var, NA
Apoptosis↑, TumCCA↓, TumCMig↓, TumMeta↓, ChemoSen↑, eff↑, eff↑, eff↓, eff↝, Dose∅, AMPK↑, p62↓, LC3II↑, Ca+2↑, Bax:Bcl2↑, CDK4↑, CDK6↑, RB1↑, EMT↓, E-cadherin↑, Vim↓, β-catenin/ZEB1↓, NF-kB↓, angioG↑, VEGF↓, TSP-1↑, MMP9↓, MMP2↓, ChemoSen↑, eff↑, ROS↑, CSCs↓, Fas↑, P53↑, BAX↑, Casp↑, β-catenin/ZEB1↓, NDRG1↑, STAT3↓, MAPK↑, ERK↑, eff↑, eff↑, eff↑,
2780- CHr,    Anti-cancer Activity of Chrysin in Cancer Therapy: a Systematic Review
- Review, Var, NA
*antiOx↑, Inflam↓, *hepatoP↑, AntiCan↑, Cyt‑c↑, Casp3↑, XIAP↓, p‑Akt↓, PI3K↑, Apoptosis↑, COX2↓, FAK↓, AMPK↑, STAT3↑, MMP↓, DNAdam↑, BAX↑, Bak↑, Casp9↑, p38↑, MAPK↑, TumCCA↑, ChemoSen↑, HDAC8↓, Wnt↓, NF-kB↓, angioG↓, BioAv↓,
2830- FIS,    Biological effects and mechanisms of fisetin in cancer: a promising anti-cancer agent
- Review, Var, NA
TumCG↓, angioG↓, *ROS↓, TumCMig↓, VEGF↓, MAPK↑, NF-kB↓, PI3K↓, Akt↓, mTOR↓, NRF2↑, HO-1↑, ROS↓, Inflam↓, ER Stress↑, ROS↑, TumCP↓, ChemoSen↑, PTEN↑, P53↑, Casp3↑, Casp8↑, Casp9↑, COX2↓, Wnt↓, EGFR↓, Mcl-1↓, survivin↓, IAP1↓, IAP2↓, PGE2↓, β-catenin/ZEB1↓, DR5↑, MMP2↓, MMP9↓, FAK↓, uPA↓, EMT↓, ERK↓, JNK↑, p38↑, PKCδ↓, BioAv↓, BioAv↑, BioAv↑,
2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,
1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumCG↑, TumMeta↑, ChemoSideEff↓, radioP↑, ChemoSen↑, *ROS↓, *SOD↑, *GSH↑, *GPx↑, *Catalase↑, Dose∅, VEGF↓, eff↑, Hif1a↓, GLUT1↑, GLUT3↑, CAIX↑, P21↑, p27↑, PTEN↑, Warburg↓, PI3K↓, Akt↓, NF-kB↓, cycD1/CCND1↓, CDK4↓, CycB/CCNB1↓, CDK4↓, MAPK↑, IGF-1R↓, STAT3↓, MMP9↓, MMP2↓, MMP13↓, E-cadherin↑, Vim↓, RANKL↓, JNK↑, Bcl-2↓, P53↑, Casp3↑, Casp9↑, BAX↑, DNArepair↑, COX2↓, IL6↓, IL8↓, NO↓, T-Cell↑, NK cell↑, Treg lymp↓, FOXP3↓, CD4+↑, TNF-α↑, Th1 response↑, BioAv↝, RadioS↑, OS↑,
3457- MF,    Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis
- Review, Var, NA
Apoptosis↑, H2O2↑, ROS↑, eff↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, TumCG↓, TumCCA↑, Apoptosis↑, TumAuto↑, Diff↑, angioG↓, TumMeta↓, EPR↑, ChemoSen↑, ROS↑, DNAdam↑, P53↑, Akt↓, MAPK↑, Casp9↑, VEGFR2↓, P-gp↓,
1890- MGO,    The Dual-Role of Methylglyoxal in Tumor Progression – Novel Therapeutic Approaches
- Review, Var, NA
AntiCan?, TumCG↓, GAPDH↓, Apoptosis↑, TumCCA↑, MAPK↑, Bcl-2↓, MMP9↓, eff↑,
2954- PL,    The metabolites from traditional Chinese medicine targeting ferroptosis for cancer therapy
- Review, Var, NA
NRF2↑, ROS↑, ER Stress↑, MAPK↑, CHOP↑, selectivity↑, Keap1↝, HO-1↑, Ferroptosis↑,
3338- QC,    Quercetin: Its Antioxidant Mechanism, Antibacterial Properties and Potential Application in Prevention and Control of Toxipathy
- Review, Var, NA - Review, Stroke, NA
*antiOx↑, *GSH↑, *ROS↓, *Dose↑, *NADPH↓, *AMP↓, *NF-kB↓, *p38↑, *MAPK↑, *SOD↑, *MDA↓, *iNOS↓, *Catalase↑, *PI3K↑, *Akt↑, *lipid-P↓, *memory↑, *radioP↑, *neuroP↑, *MDA↓,
3063- RES,    Resveratrol: A Review of Pre-clinical Studies for Human Cancer Prevention
- Review, Var, NA
*Inflam↓, *antiOx↑, *AntiAg↑, *chemoPv↑, ChemoSen↑, BioAv↑, Half-Life↝, COX2↓, cycD1/CCND1↓, CDK2↓, CDK4↓, CDK6↓, P21↑, MMP9↓, NF-kB↓, Telomerase↓, PSA↓, MAPK↑, P53↑,
1722- SFN,    Sulforaphane as an anticancer molecule: mechanisms of action, synergistic effects, enhancement of drug safety, and delivery systems
- Review, Var, NA
TumCCA↑, CYP1A1↓, CYP3A4↓, Cyt‑c↑, Casp9↑, Apoptosis↑, ROS↑, MAPK↑, P53↑, BAX↑, ChemoSen↑, HDAC↓, GSH↓, HO-1↑,
2106- TQ,    Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy
- Review, Var, NA
Apoptosis↑, TumCCA↑, ROS↑, *Catalase↑, *SOD↑, *GR↑, *GSTA1↓, *GPx↑, *H2O2↓, *ROS↓, *lipid-P↓, *HO-1↑, p‑Akt↓, AMPKα↑, NK cell↑, selectivity↑, Dose↝, eff↑, GSH↓, eff↓, P53↑, p‑STAT3↓, PI3K↑, MAPK↑, GSK‐3β↑, ChemoSen↑, RadioS↑, BioAv↓, NRF2↑,
3411- TQ,    Anticancer and Anti-Metastatic Role of Thymoquinone: Regulation of Oncogenic Signaling Cascades by Thymoquinone
- Review, Var, NA
p‑STAT3↓, cycD1/CCND1↓, JAK2↓, β-catenin/ZEB1↓, cMyc↓, MMP7↓, MET↓, p‑Akt↓, p‑mTOR↓, CXCR4↓, Bcl-2↓, BAX↑, ROS↑, Cyt‑c↑, Twist↓, Zeb1↓, E-cadherin↑, p‑p38↑, p‑MAPK↑, ERK↑, eff↑, ERK↓, TumCP↓, TumCMig↓, TumCI↓,
3559- TQ,    Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease
- Review, AD, NA - Review, Var, NA
*antiOx↑, *Inflam↓, *AChE↓, AntiCan↑, *cardioP↑, *RenoP↑, *neuroP↑, *hepatoP↑, TumCG↓, Apoptosis↑, PI3K↓, Akt↑, TumCCA↑, angioG↓, *NF-kB↓, *TLR2↓, *TLR4↓, *MyD88↓, *TRIF↓, *IRF3↓, *IL1β↓, *IL6↓, *IL12↓, *NRF2↑, *COX2↓, *VEGF↓, *MMP9↓, *cMyc↓, *cycD1/CCND1↓, *TumCP↓, *TumCI↓, *MDA↓, *TGF-β↓, *CRP↓, *Casp3↓, *GSH↑, *IL10↑, *iNOS↑, *lipid-P↓, *SOD↑, *H2O2↓, *ROS↓, *LDH↓, *Catalase↑, *GPx↑, *AChE↓, *cognitive↑, *MAPK↑, *JNK↑, *BAX↓, *memory↑, *Aβ↓, *MMP↑,

Showing Research Papers: 1 to 21 of 21

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ATF3↑, 1,   Catalase↓, 1,   CYP1A1↓, 1,   Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 2,   GSR↑, 1,   H2O2↑, 1,   HO-1↑, 5,   Iron↑, 1,   Keap1↝, 1,   lipid-P?, 1,   lipid-P↑, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 4,   ROS↓, 2,   ROS↑, 14,   SIRT3↑, 2,   SOD↓, 1,   Trx1↑, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 2,   mitResp↓, 1,   MMP↓, 4,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   CAIX↑, 1,   cMyc↓, 1,   CYP3A4↓, 1,   GAPDH↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   NADPH↑, 1,   PPARα↓, 1,   TCA↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 6,   Akt↑, 1,   p‑Akt↓, 4,   APAF1↑, 1,   Apoptosis↑, 12,   Bak↑, 1,   BAX↑, 8,   Bax:Bcl2↑, 1,   Bcl-2↓, 6,   BIM↑, 1,   Casp↑, 3,   Casp3↑, 5,   cl‑Casp3↑, 1,   Casp8↑, 2,   Casp9↑, 6,   cl‑Casp9↑, 1,   proCasp9↓, 1,   Chk2↓, 1,   Cyt‑c↑, 6,   DR4↑, 1,   DR5↑, 4,   Fas↑, 1,   Ferroptosis↑, 2,   HEY1↓, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   IAP2↓, 1,   JNK↑, 5,   MAPK↑, 17,   p‑MAPK↑, 1,   Mcl-1↓, 2,   MDM2↓, 1,   p27↑, 1,   p38↑, 7,   p‑p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   RET↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

H3↑, 1,   other↑, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 3,   eIF2α↓, 1,   ER Stress↑, 4,   HSP90↓, 2,   HSPs↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   BNIP3↑, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↑, 2,   DNArepair↑, 1,   P53↑, 9,   PARP↑, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 5,   CDK4↓, 6,   CDK4↑, 1,   cycA1/CCNA1↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 2,   P21↑, 3,   RB1↑, 1,   p‑RB1↓, 2,   TumCCA↓, 1,   TumCCA↑, 10,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   cMET↓, 1,   CSCs↓, 3,   Diff↑, 1,   EMT↓, 6,   ERK↓, 2,   ERK↑, 2,   p‑ERK↓, 2,   FOXO3↑, 1,   GSK‐3β↑, 1,   HDAC↓, 1,   HDAC8↓, 1,   IGF-1R↓, 1,   Let-7↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 2,   NOTCH1↓, 1,   PI3K↓, 6,   PI3K↑, 2,   PTEN↑, 2,   SOX2↓, 1,   STAT3↓, 6,   STAT3↑, 1,   p‑STAT3↓, 3,   TOP1↓, 2,   TOP2↑, 1,   TumCG↓, 4,   TumCG↑, 1,   Wnt↓, 5,  

Migration ⓘ

AP-1↓, 2,   Ca+2↑, 3,   E-cadherin↑, 4,   ER-α36↓, 1,   FAK↓, 3,   LAMs↓, 1,   MALAT1↓, 1,   MET↓, 1,   miR-200b↑, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 6,   MMP7↓, 1,   MMP9↓, 8,   MMPs↓, 1,   N-cadherin↓, 2,   PDGF↓, 1,   PKCδ↓, 1,   Slug↓, 1,   Snail↓, 2,   Treg lymp↓, 1,   TSP-1↑, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 3,   TumMeta↓, 2,   TumMeta↑, 1,   Twist↓, 2,   uPA↓, 3,   Vim↓, 4,   Zeb1↓, 1,   β-catenin/ZEB1↓, 7,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   angioG↑, 1,   ATF4↑, 1,   EGFR↓, 1,   p‑EGFR↓, 1,   EPR↑, 1,   Hif1a↓, 1,   NO↓, 1,   PDGFR-BB↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 8,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,   GLUT3↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 6,   CXCR4↓, 2,   FOXP3↓, 1,   IKKα↓, 1,   IL1↓, 1,   IL1α↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 3,   JAK2↓, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 10,   NK cell↑, 2,   PGE2↓, 1,   PSA↓, 1,   T-Cell↑, 1,   Th1 response↑, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,   CDK6↑, 1,   RANKL↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 5,   BioAv↝, 2,   ChemoSen↑, 12,   Dose↑, 1,   Dose↝, 2,   Dose∅, 2,   eff↓, 3,   eff↑, 19,   eff↝, 1,   Half-Life↓, 1,   Half-Life↝, 1,   RadioS↑, 2,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   ascitic↓, 1,   E6↓, 2,   E7↓, 2,   EGFR↓, 1,   p‑EGFR↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 2,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 5,   AntiCan?, 1,   AntiTum↑, 1,   cardioP↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   ChemoSideEff↓, 1,   hepatoP↑, 1,   NDRG1↑, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 254

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 6,   Catalase↑, 6,   GPx↑, 3,   GPx1↑, 1,   GPx4↑, 1,   GSH↑, 4,   GSR↑, 1,   GSTA1↓, 1,   GSTs↑, 1,   H2O2↓, 2,   HO-1↑, 1,   lipid-P↓, 4,   MDA↓, 3,   NRF2↑, 4,   Prx↑, 1,   ROS↓, 6,   SOD↑, 5,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,  

Core Metabolism/Glycolysis ⓘ

AMP↓, 1,   cMyc↓, 1,   LDH↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Akt↑, 1,   BAX↓, 1,   Casp3?, 1,   Casp3↓, 1,   iNOS↓, 1,   iNOS↑, 1,   JNK↑, 1,   MAPK↑, 3,   p38↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  

Migration ⓘ

AntiAg↑, 2,   Ca+2↝, 1,   MMP9↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL10↑, 1,   IL12↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   MyD88↓, 1,   NF-kB↓, 3,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,   TRIF↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Dose↑, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   chemoPv↑, 1,   cognitive↑, 1,   hepatoP↑, 3,   memory↑, 2,   neuroP↑, 3,   radioP↑, 1,   RenoP↑, 1,   toxicity?, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

IRF3↓, 1,  
Total Targets: 76

Scientific Paper Hit Count for: MAPK, mitogen-activated protein kinase
3 Thymoquinone
2 Allicin (mainly Garlic)
2 Ashwagandha(Withaferin A)
2 Magnetic Fields
1 Betulinic acid
1 Boswellia (frankincense)
1 Caffeic acid
1 Propolis -bee glue
1 Chrysin
1 Fisetin
1 Luteolin
1 Melatonin
1 Methylglyoxal
1 Piperlongumine
1 Quercetin
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
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#:181  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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