MEK Cancer Research Results

MEK, Mitogen-Activated Protein Kinase Kinase: Click to Expand ⟱
Source:
Type: protein kinase
MEK (Mitogen-Activated Protein Kinase Kinase) is a protein kinase that plays a crucial role in the regulation of cell growth, differentiation, and survival.
MEK is often overexpressed or mutated, leading to the activation of downstream signaling pathways that promote cell growth, survival, and metastasis. MEK inhibitors have been developed as a therapeutic strategy to target cancer cells and inhibit their growth.
Scientific Papers found: Click to Expand⟱
144- CUR,  Bical,    Combination of curcumin and bicalutamide enhanced the growth inhibition of androgen-independent prostate cancer cells through SAPK/JNK and MEK/ERK1/2-mediated targeting NF-κB/p65 and MUC1-C
- in-vitro, Pca, PC3 - in-vitro, PC, DU145 - in-vitro, PC, LNCaP
p‑ERK↑, ERK1/2
p‑JNK↓, phosphorylation
MUC1↓, MUC1-C protein expression
p65↓,
AR↓, bicalutamide, an androgen receptor antagonist, inhibited cell growth in dose- and time-dependent fashion in PC3 and LNCaP cells.
TumCG↓,
MEK↑, curcumin inhibits the growth of androgen-independent prostate cancer cells through MEK/ERK1/2 and SAPK/JNK-mediated inhibition of p65, followed by reducing expression of MUC1-C protein.
SAPK↑, through activation of MEK/ERK/12 and SAPK/JNK

6736- Dipy,    Nucleoside Transport Inhibition by Dipyridamole Prevents Angiogenesis Impairment by Homocysteine and Adenosine
*other↝, he results showed that dipyridamole restored the extracellular adenosine and intracellular S-adenosylhomocysteine concentrations disrupted by the combination of homocysteine and adenosine.
*p‑MEK↑, dipyridamole induced the phosphorylation of mitogen-activated protein kinase kinase (MEK) and extracellular signal-regulated kinases (ERK)
*ERK↑,
*angioG↑, Dipyridamole protected against impaired angiogenesis caused by homocysteine and adenosine, at least in part, by activating the MEK/ERK signalling pathway, and this could be associated with its effects in suppressing intracellular S-adenosylhomocystei

7772- IBC,    Isobavachalcone inhibits acute myeloid leukemia: Potential role for ROS-dependent mitochondrial apoptosis and differentiation
- vitro+vivo, AML, NA
Apoptosis↑, Isobavachalcone (IBC) has been shown to induce apoptosis and differentiation of acute myeloid leukemia (AML) cells.
Diff↑,
tumCV↓, Herein, IBC exhibited significant inhibition on the cell viability, proliferation, and the colony formation ability of AML cells.
TumCP↓,
MMP↓, IBC induced mitochondrial apoptosis evidenced by reduced mitochondrial membrane potential, increased Bax level, decreased Bcl-2, Bcl-xL, and Mcl-1 levels, elevated cytochrome c level in the cytosol and increased cleavage of caspase-9, caspase-3, and
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp9↑,
cl‑PARP↑,
p‑MEK↑, increase of the phosphorylation of MEK and ERK and the C/EBPα expression as well as the C/EBPβ LAP/LIP isoform ratio, which was significantly reversed by U0126, a specific inhibitor of MEK
p‑ERK↑,
ROS↑, Notably, IBC enhanced the intracellular ROS level.
eff↓, More importantly, IBC-induced apoptosis and differentiation of HL-60 cells were significantly mitigated by NAC.

4704- PTS,  Cisplatin,    Pterostilbene Sensitizes Cisplatin-Resistant Human Bladder Cancer Cells with Oncogenic HRAS
- in-vitro, Bladder, NA
PI3K↓, Pterostilbene-induced autophagy in T24 cells was paralleled by inhibition of class I PI3K/mTOR/p70S6K as well as activation of MEK/ERK (a RAS target) and class III PI3K pathways.
mTOR↓,
P70S6K↓,
MEK↑,
ERK↑,
ChemoSen↑, Animal study data confirmed that pterostilbene enhanced cytotoxicity of cisplatin plus gemcitabine.
TumAuto↑, Pterostilbene-Enhanced Cytotoxic Response to Food and Drug Administration (FDA)-Approved Anticancer Drugs Was Indeed Associated with an Induction of Autophagy


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MEK↑, 2,   p‑MEK↑, 1,   MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   p‑JNK↓, 1,   Mcl-1↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,   SAPK↑, 1,  

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

Diff↑, 1,   ERK↑, 1,   p‑ERK↑, 2,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

MUC1↓, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

p65↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Mitochondria & Bioenergetics(tgid=3) ⓘ

p‑MEK↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

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

ERK↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,  
Total Targets: 4

Scientific Paper Hit Count for: MEK, Mitogen-Activated Protein Kinase Kinase
1 Curcumin
1 Bicalutamide
1 Dipyridamole
1 Isobavachalcone
1 Pterostilbene
1 Cisplatin
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#:860  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page