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.


GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.

Scientific Papers found: Click to Expand⟱
248- AL,    Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway
- in-vitro, GBM, U87MG
Bcl-2↓, BAX↑, MAPK↑, ERK↑, ROS↑, p38↑, JNK↑,
235- AL,    Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway
- in-vitro, GBM, U87MG
Apoptosis↑, Bcl-2↓, BAX↑, MAPK↑, p‑ERK↑, ROS↑, eff↓,
2082- HNK,    Revealing the role of honokiol in human glioma cells by RNA-seq analysis
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
AntiCan↑, TumCP↑, TumAuto↑, Apoptosis↑, *BioAv↑, *neuroP↑, *NF-kB↑, MAPK↑, GPx4↑, Tf↑, BAX↑, Bcl-2↓, antiOx↑, Hif1a↓, Ferroptosis↑,
5099- JG,    Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK
- vitro+vivo, GBM, LN229 - vitro+vivo, GBM, T98G
Ferroptosis↑, p‑MAPK↑, NRF2↓, GPx4↓, TumPF↓, Apoptosis↑, ROS↑, GSH↓, lipid-P↑, Ki-67↓, TumCG↓,

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

antiOx↑, 1,   Ferroptosis↑, 2,   GPx4↓, 1,   GPx4↑, 1,   GSH↓, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↑, 3,  

Metal & Cofactor Biology

Tf↑, 1,  

Cell Death

Apoptosis↑, 3,   BAX↑, 3,   Bcl-2↓, 3,   Ferroptosis↑, 2,   JNK↑, 1,   MAPK↑, 3,   p‑MAPK↑, 1,   p38↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State

ERK↑, 1,   p‑ERK↑, 1,   TumCG↓, 1,  

Migration

Ki-67↓, 1,   TumCP↑, 1,   TumPF↓, 1,  

Angiogenesis & Vasculature

Hif1a↓, 1,  

Drug Metabolism & Resistance

eff↓, 1,  

Clinical Biomarkers

Ki-67↓, 1,  

Functional Outcomes

AntiCan↑, 1,  
Total Targets: 28

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling

NF-kB↑, 1,  

Drug Metabolism & Resistance

BioAv↑, 1,  

Functional Outcomes

neuroP↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: MAPK, mitogen-activated protein kinase
2 Allicin (mainly Garlic)
1 Honokiol
1 Juglone
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:27  Cells:%  prod#:%  Target#:181  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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