JNK Cancer Research Results

JNK, c-Jun N-terminal kinase (JNK): Click to Expand ⟱
Source:
Type:
JNK acts synergistically with NF-κB, JAK/STAT, and other signaling molecules to exert a survival function. Janus signaling promotes cancer cell survival.
JNK, or c-Jun N-terminal kinase, is a member of the mitogen-activated protein kinase (MAPK) family. It plays a crucial role in various cellular processes, including cell proliferation, differentiation, and apoptosis (programmed cell death). JNK is activated in response to various stress signals, such as UV radiation, oxidative stress, and inflammatory cytokines.
JNK activation can promote apoptosis in cancer cells, acting as a tumor suppressor. However, in other contexts, it can promote cell survival and proliferation, contributing to tumor progression.

JNK is often unregulated in cancers, leading to increased cancer cell proliferation, survival, and resistance to apoptosis. This activation is typically associated with poor prognosis and aggressive tumor behavior.
Ovarian, Ovarian Cancer: Click to Expand ⟱
Ovarian Cancer
Scientific Papers found: Click to Expand⟱
2791- CHr,    Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction
- in-vitro, Ovarian, OV90
TumCP↓, TumCD↑, ROS↑, Ca+2↑, MMP↓, MAPK↑, PI3K↑, p‑Akt↑, PCNA↓, p‑p70S6↑, p‑ERK↑, p38↑, JNK↑, DNAdam↑, TumCCA↑, chemoP↑,
1271- NCL,    Niclosamide inhibits ovarian carcinoma growth by interrupting cellular bioenergetics
- vitro+vivo, Ovarian, SKOV3
Wnt/(β-catenin)↓, mTOR↓, STAT3↓, NF-kB↓, NOTCH↓, TumCG↓, Apoptosis↑, MEK↓, ERK↓, mitResp↓, Glycolysis↓, ROS↑, JNK↑,
4943- PEITC,    Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activation
- in-vitro, Ovarian, OVCAR-3
TumCD↑, TumCP↓, Apoptosis↑, Casp3↑, Casp9↑, Bcl-2↓, BAX↑, Akt↓, ERK↓, cMyc↓, p38↑, JNK↑, eff↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   mitResp↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↑, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   JNK↑, 3,   MAPK↑, 1,   p38↑, 2,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

p‑p70S6↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 2,   p‑ERK↑, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↑, 1,   STAT3↓, 1,   TumCG↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↑, 1,   TumCP↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 34

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: JNK, c-Jun N-terminal kinase (JNK)
1 Chrysin
1 Niclosamide (Niclocide)
1 Phenethyl isothiocyanate
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:20  Cells:%  prod#:%  Target#:168  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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