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.
Scientific Papers found: Click to Expand⟱
3778- FA,    Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer’s Disease: A Narrative Review
- Review, AD, NA
*neuroP↑, it seems to ameliorate AD pathology by preventing neurodegeneration in several brain regions;
*Aβ↓, it has been shown to inhibit Aβ oligomer aggregations and to exert antioxidant, anti-inflammatory, and anti-apoptotic effects
*antiOx↑,
*Inflam↓,
*ROS↓, ability of ferulic acid to prevent oxidative stress
*NF-kB↓, inhibition of the nuclear factor kappa-B (NF-κ B),
*NLRP3↓, it also inhibited the NLR pyrin domain-containing protein 3 (NLRP3) inflammasome
*iNOS↓, A down-regulation by ferulic acid of proinflammatory molecules, such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1), has been observe
*COX2↓,
*TNF-α↓,
*IL1β↓,
*VCAM-1↓,
*ICAM-1↓,
*p‑MAPK?, inhibiting the phosphorylation of MAPKs, including p38 and c-Jun N-terminal kinase (JNK),
*hepatoP↑, ferulic acid reduces the liver damage induced by acetaminophen in a mouse model of hepatotoxicity by inhibiting the expression of toll like receptor 4 (TLR4),
*TLR4↓,
*PPARγ↑, ferulic acid upregulated PPARγ and Nrf2 expression in renal cells,
*NRF2↑,
*Fenton↓, Ferulic acid may also inhibit the generation of reactive oxygen species (ROS) through the Fenton reaction, acting as a chelator of metals (i.e., Fe and Cu),
*IronCh↑,
*MDA↓, a lowering in the levels of malondialdehyde (MDA), a lipid peroxidation marker
*HO-1↑, Ferulic acid has been found able to upregulate HO-1, thus increasing the production of bilirubin, which acts as an efficient ROS scavenger,
*Bil↑,
*GCLC↑, (GCLC), glutamate-cysteine ligase regulatory subunit (GCLM), and NADPH quinone oxidoreductase-1 (NQO1) were induced by ferulic acid
*GCLM↑,
*NQO1↑,
*GutMicro↑, ferulic acid esterified forms have been shown to act as a prebiotic, since they stimulate the growth of eubacteria, such as Lactobacilli and Bifidobacteria, in the human gastrointestinal tract, so preserving the homeostasis of gut microbiota,
*SOD↑, Indeed, it prevented membrane damage, scavenged free radicals, increased SOD activity, and decreased the intracellular free Ca2+ levels, lipid peroxidation, and the release of prostaglandin E2 (PGE2);
*Ca+2↓,
*lipid-P↓,
*PGE2↓,

7140- GI,    Benefits of Ginger and Its Constituent 6-Shogaol in Inhibiting Inflammatory Processes
- Review, Var, NA
*Dose↝, 6-Shogaol is formed from 6-gingerol by dehydration and represents one of the main bioactive principles in dried ginger rhizomes.
*Inflam↓, In vitro and in vivo, 6-shogaol reduced inflammatory mediator systems such as COX-2 or iNOS, affected NFκB and MAPK signaling, and increased levels of cytoprotective HO-1.
*COX2↓,
*iNOS↓,
*NF-kB↓,
*MAPK?,
*HO-1↑,
*PGE2↓, Rat/saline administration 50 and 500 mg/kg extract oral or i.p. Reduced PGE2 serum levels
*TNF-α↓, 25, 50, 100 and 200 mg/kg extract oral Reduced carrageenan-induced paw volume, levels of PGE2, TNF, IL-6, IL-1β, IFNγ, MCP-1, MIP-2, RANTES, and MPO activity and NO levels
*IL6↓,
*IL1β↓,
*IFN-γ↓,
*MCP1/CCL2↓,
*MIP2↓,
*RANTES↓,
*MPO↓,
*NO↓,
*Stroke↓, Therefore, the authors of this study suggest a potential benefit of 6-shogaol for the prevention of stroke [51].
*BrainVol↑, The daily oral administration of 6-shogaol (5 and 20 mg/kg) resulted in protection against transient focal cerebral ischemia, as indicated by a significant reduction of brain infarct volume and production of malondialdehyde (MDA) and of ROS after MCA
*MDA↓,
*ROS↓,
*GSH↑, 6-shoagol treatment resulted in an increased amount of glutathione (GSH) in H2O2-induced HepG2 cells
*NRF2↑, As H2O2-triggered Nrf2 degradation was recovered by 6-shogaol,
*antiOx↑, 6-Shogaol exhibits a stronger antioxidative activity than its homologues
NLRP3↓, 6-shogaol (20 µM) effectively inhibited total protein levels of NLRP3 and pro-IL-1β after a combined LPS and ATP-activated protein up-regulation
HDAC1↓, The LPS-caused induction of HDAC1 protein levels was reduced by 6-shogaol


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


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

HDAC1↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Bil↑, 1,   Fenton↓, 1,   GCLC↑, 1,   GCLM↑, 1,   GSH↑, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 2,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 2,   SOD↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 2,   MAPK?, 1,   p‑MAPK?, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 2,   ICAM-1↓, 1,   IFN-γ↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam↓, 2,   MCP1/CCL2↓, 1,   MIP2↓, 1,   NF-kB↓, 2,   PGE2↓, 2,   RANTES↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BrainVol↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Bil↑, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 45

Scientific Paper Hit Count for: MAPK, mitogen-activated protein kinase
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:%  Cells:%  prod#:%  Target#:181  State#:%  Dir#:0
  wNotes=on  sortOrder:rid,rpid

 

Home Page