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.


Thyroid, Thyroid: Click to Expand ⟱
Thyroid


Scientific Papers found: Click to Expand⟱
5505- Ba,    Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway
- in-vitro, Thyroid, NA
ERK↓, PI3K↓, Akt↓, Apoptosis↑, TumAuto↑, NF-kB↑, MEK↓,
1276- SIL,    Silibinin inhibits TPA-induced cell migration and MMP-9 expression in thyroid and breast cancer cells
- in-vitro, BC, NA - in-vitro, Thyroid, NA
TumCMig↓, MMP9↓, p‑MEK↓, p‑ERK↓,

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:


Mitochondria & Bioenergetics

MEK↓, 1,   p‑MEK↓, 1,  

Cell Death

Akt↓, 1,   Apoptosis↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State

ERK↓, 1,   p‑ERK↓, 1,   PI3K↓, 1,  

Migration

MMP9↓, 1,   TumCMig↓, 1,  

Immune & Inflammatory Signaling

NF-kB↑, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MEK, Mitogen-Activated Protein Kinase 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:43  Cells:%  prod#:%  Target#:860  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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