ERK Cancer Research Results

ERK, ERK signaling: Click to Expand ⟱
Source:
Type:
MAPK3 (ERK1)
ERK proteins are kinases that activate other proteins by adding a phosphate group. An overactivation of these proteins causes the cell cycle to stop.
The extracellular signal-regulated kinase (ERK) signaling pathway is a crucial component of the mitogen-activated protein kinase (MAPK) signaling cascade, which plays a significant role in regulating various cellular processes, including proliferation, differentiation, and survival. high levels of phosphorylated ERK (p-ERK) in tumor samples may indicate active ERK signaling and could correlate with aggressive tumor behavior

EEk singaling is frequently activated and is often associated with aggressive tumor behavior, treatment resistance, and poor outcomes.
Scientific Papers found: Click to Expand⟱
1157- And,    Andrographolide suppresses the migratory ability of human glioblastoma multiforme cells by targeting ERK1/2-mediated matrix metalloproteinase-2 expression
- in-vitro, GBM, GBM8401 - in-vitro, GBM, U251
TumCI↓,
TumCMig↓,
MMP2↓,
ERK↝, combination of andrographolide and an ERK inhibitor might be a good strategy for preventing GBM metastasis

5182- BBR,    Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-κB, u-PA and MMP-2 and -9
- in-vitro, SCC, SCC4
TumCMig↓, berberine inhibited migration and invasion of human SCC-4 tongue squamous carcinoma cells
TumCI↓,
p‑JNK↝, This action was mediated by the p-JNK, p-ERK, p-p38, IκK and NF-κB signaling pathways resulting in inhibition of MMP-2 and -9
p‑ERK↝,
p‑p38↝,
IKKα↝,
NF-kB↝,
MMP2↓,
MMP9↓,

5856- CAP,    Potential of capsaicin as a combinatorial agent to overcome chemoresistance and to improve outcomes of cancer therapy
- Review, Var, NA
ChemoSen↑, has garnered significant interest for its potential role as a combinatorial and chemosensitizing agent in cancer therapy
Apoptosis↑, CAPS enhanced the efficacy of various anticancer agents by promoting apoptosis, modulating autophagy and inhibiting angiogenesis, tumor growth, and metastasis.
TumAuto↑,
angioG↓,
TumCG↓,
TumMeta↓,
P-gp↝, CAPS modulated critical regulators of chemoresistance, such as P-glycoprotein (P-gp), extracellular signal-regulated kinase (ERK), nuclear factor-kappa B (NF-κB) pathway, and signal transducer and activator of transcription 3 (STAT3) pathway
ERK↝,
NF-kB↝,
STAT3↝,
eff↑, combination with chemotherapeutic agents, CAPS has been shown to improve treatment efficacy at lower drug concentrations.

2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, PEMFs act on the cell, it will firstly change the cell membrane transport capacity, osmotic potential and ionic valves
p‑ERK↝, Also, it will cause changes in mitochondrial protein profile, decrease mitochondrial phosphor-ERK (extracellular-signal-regulated kinase), p53, and cytochrome c, and activate OxPhos.
P53↝,
Cyt‑c↝,
OXPHOS↑,
Apoptosis↑, PEMFs decreases cellular stress factors, increase energy demand, this series of reactions will eventually lead to apoptosis.
ROS↑, The introduction of PEFs and PEMFs can improve the penetration efficiency of ROS, not only reduce the concentration of drugs, but also reduce the irradiation dose of CAP, w

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↓,


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   OXPHOS↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 3,   Casp3↑, 1,   cFLIP↓, 1,   Cyt‑c↝, 1,   p‑JNK↝, 1,   MAPK↝, 1,   p‑p38↝, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

P53↑, 1,   P53↝, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↝, 3,   p‑ERK↝, 2,   mTOR↓, 1,   STAT3↓, 1,   STAT3↝, 1,   TumCG↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

MMP2↓, 3,   MMP9↓, 1,   MMP9:TIMP1↓, 1,   MMPs↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IKKα↝, 1,   IL10↓, 1,   IL6↓, 1,   NF-kB↝, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ERK, ERK signaling
1 Andrographis
1 Berberine
1 Capsaicin
1 Magnetic Fields
1 Quercetin
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#:105  State#:%  Dir#:4
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