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⟱
6461- 1,8-Cin,    1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases
- Review, AD, NA - Review, Var, NA
*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.

171- Api,    Apigenin in cancer therapy: anti-cancer effects and mechanisms of action
- Review, Var, NA
PI3K/Akt↓,
NF-kB↓,
CK2↓,
FOXO↓,
MAPK↝, modulation of MAPKs by apigenin contributed to apigenin-induced cell cycle arrest at G0/G1 phase
ERK↓, p-ERK1/2,
p‑JAK↓, phosphorylation
Wnt/(β-catenin)↓,
ROS↑, accumulation of reactive oxygen species (ROS) production, leading to induction of DNA damage
CDC25↓,
p‑STAT↓,
DNAdam↑,

726- Bor,    Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still Open
- Review, NA, NA
NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,

6007- CGA,    A Comprehensive View on the Impact of Chlorogenic Acids on Colorectal Cancer
- Review, CRC, NA
antiOx↑, They are best known for their high concentration in coffee and other dietary sources and the antioxidant properties that they exhibit.
TumCCA↑, this review aims to enable a better understanding of the modes of action of chlorogenic acids in combating carcinogenesis, with a focus on cell cycle arrest, the induction of apoptosis, and the modulation of Wnt, Pi3K/Akt, and MAPK
Apoptosis↑,
Wnt↝,
PI3K↝,
MAPK↝,
ROS↓, CGAs have demonstrated significant reactive oxygen species (ROS) scavenging potential through two direct mechanisms: hydrogen atom transfer (HAT) and radical adduct formation (RAF)
BioAv↝, bioavailability of CGAs in humans involves a complex process of digestion, absorption, and metabolism (Figure 7), primarily occurring within the stomach, small and large intestines, governed by the interplay between host enzymes and gut microbiota
P53↑, ↑ p53, ↑ p21, ↑ p18, ↑ CDKI, ↓ cyclin-D1, ↑ G1 cell population
P21↑,
CDK1↑,
Ki-67↓, ↓ Ki-67
Ca+2↑, ↑ Ca2+ levels Caco-2—cell culture
p‑Akt↓, ↓ p-AKT, ↓ mTOR
mTOR↓,
GSH↑, ↑ GSH, ↑ Nrf-2, ↑ HO-1 Caco-2—cell culture
NRF2↑,
HO-1↑,
COX2↓, ↓ COX-2, ↓ TNF-α, ↓ IL-1β, ↓ IL-6 LPS-induced SW480—cell culture
TNF-α↓,
IL1β↓,
IL6↓,

3927- PTS,    Effects of Pterostilbene on Cardiovascular Health and Disease
- Review, AD, NA - Review, Stroke, NA
*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke

910- QC,    The Anti-Cancer Effect of Quercetin: Molecular Implications in Cancer Metabolism
tumCV↓,
Apoptosis↑,
PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
Wnt/(β-catenin)↓, reducing β-catenin
MAPK↝,
ERK↝, ERK1/2
TumCCA↑, cell cycle arrest at the G1 phase
H2O2↑,
ROS↑,
TumAuto↑,
MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
P53↑,
Casp3↑,
Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
cFLIP↓,
IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
IL10↓,
lactateProd↓,
Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
PKM2↓,
GLUT1↓,
COX2↓,
VEGF↓,
OCR↓,
ECAR↓,
STAT3↓,
MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
MMP9:TIMP1↓,
mTOR↓,

6047- SeNPs,  CGA,    Synergistic anti-oxidative/anti-inflammatory treatment for acute lung injury with selenium based chlorogenic acid nanoparticles through modulating Mapk8ip1/MAPK and Itga2b/PI3k-AKT axis
- in-vitro, Nor, NA
*Dose↝, chlorogenic acid, a polyphenol commonly found in herb, had been effectively conjugated with human serum albumin and coated on selenium nanoparticles (Se NPs) to create CHSe NPs.
*SOD↑, CHSe NPs exhibited superoxide dismutase(SOD) like and glutathione peroxidase(GPX) like activities, effectively scavenging various types of reactive oxygen species (ROS), and inhibited the inflammatory response of macrophages.
*GPx↑,
*ROS↓,
*Inflam↓,
*MAPK↝, CHSe NPs synergistically exert antioxidant and anti-inflammatory effects by regulating the MAPK signaling pathway and PI3K-Akt signaling pathway, showing enormous potential in the treatment of ALI.
*PI3K↝,

4203- SIL,    Unlocking the Neuroprotective Potential of Silymarin: A Promising Ally in Safeguarding the Brain from Alzheimer’s Disease and Other Neurological Disorders
- Review, NA, NA
*MAPK↝, Silymarin utilizes a range of molecular mechanisms, including modulation of MAPK, AMPK, NF-κB, mTOR, and PI3K/Akt pathways
*AMPK↝,
*NF-kB↓,
*mTOR↝,
*PI3K↝,
*Akt↝,
*BioAv↝, silymarin faces challenges related to bioavailability and aqueous solubility, hindering its development as a clinical drug
*memory↑, silymarin dose-dependently improves the memory and expression of BDNF in TBI-induced mice along with a significant reduction in the level of glutamate and TNF-α, affirming that silymarin could be a potential therapeutic agent for addressing cognitiv
*BDNF↑,
*TNF-α↓,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↓, 1,   GSH↓, 1,   GSH↑, 1,   H2O2↑, 1,   HO-1↑, 1,   MDA↑, 1,   MFN2↑, 1,   NRF2↑, 2,   ROS↓, 1,   ROS↑, 4,   SAM-e↝, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   p‑MEK↓, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   NAD↝, 1,   PI3K/Akt↓, 1,   PI3K/Akt↝, 1,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 2,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BID↑, 1,   Casp3↑, 2,   cl‑Casp3⇅, 1,   Casp9↑, 2,   cFLIP↓, 1,   CK2↓, 1,   Cyt‑c↑, 1,   MAPK↝, 5,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ATF6↑, 1,   eIF2α↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 3,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↑, 1,   Cyc↓, 1,   P21↓, 1,   P21↑, 1,   TumCCA↑, 3,  

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

BRAF↝, 1,   ERK↓, 1,   ERK↝, 1,   p‑ERK↓, 1,   FOXO↓, 1,   IGF-1↓, 1,   mTOR↓, 2,   mTOR↝, 1,   PI3K↝, 1,   PTEN↝, 1,   p‑STAT↓, 1,   STAT3↓, 1,   Wnt↝, 1,   Wnt/(β-catenin)↓, 2,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9:TIMP1↓, 1,   MMPs↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↑, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 3,   IL1↓, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 3,   p‑JAK↓, 1,   NF-kB↓, 1,   PSA↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRAF↝, 1,   IL6↓, 3,   Ki-67↓, 1,   PSA↓, 1,  
Total Targets: 92

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,   TRPA1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 3,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↝, 1,   LDL↓, 1,   NADPH↓, 1,   NADPH↑, 1,   PPARα↑, 1,   PPARγ↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↝, 1,   MAPK↝, 3,  

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

GSK‐3β↓, 1,   mTOR↝, 1,   PI3K↝, 2,  

Migration(tgid=13) ⓘ

E-sel↓, 1,   MMPs↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   IL1β↓, 2,   IL4↓, 1,   IL8↓, 1,   Inflam↓, 3,   MCP1↓, 1,   NF-kB↓, 3,   PGE2↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,   tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   BioAv↝, 1,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,   toxicity↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,  
Total Targets: 51

Scientific Paper Hit Count for: MAPK, mitogen-activated protein kinase
2 Chlorogenic acid
1 1,8-Cineole
1 Apigenin (mainly Parsley)
1 Boron
1 Pterostilbene
1 Quercetin
1 Selenium NanoParticles
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:%  Cells:%  prod#:%  Target#:181  State#:%  Dir#:4
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