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.
HNSCC, Head and Neck Squamous Cell Carcinoma: Click to Expand ⟱
Head and Neck Squamous Cell Carcinoma
Scientific Papers found: Click to Expand⟱
5697- BRU,    Brusatol, a Nrf2 Inhibitor Targets STAT3 Signaling Cascade in Head and Neck Squamous Cell Carcinoma
- in-vitro, HNSCC, NA
NRF2↓, STAT3↓, proCasp3↑, cl‑PARP↑, Bcl-2↓, Bcl-xL↓, survivin↓, Hif1a↓, cMyc↓, JNK↑, MAPK↑, tumCV↓, ROS∅,
6901- FIS,    Fisetin induces G2/M phase arrest and caspase-mediated cleavage of p21Cip1 and p27Kip1 leading to apoptosis and tumor growth inhibition in HNSCC
- in-vivo, HNSCC, CAL33
TumCG↓, TumCD↑, selectivity↑, TumCCA↑, CDC25↓, CDK1↓, CycB/CCNB1↓, P53↑, DNAdam↑, Apoptosis↑, γH2AX↑, cl‑PARP↑, other↝, JNK↑, PI3K↓, Akt↓, ERK↓, EGFR↓, STAT3↓, TumAuto↑, Dose↝, TumVol↓, Ki-67↓, cl‑Casp3↑, P21↓, p27/CDKN1B↓,

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:


Redox & Oxidative Stress(tgid=1) ⓘ

NRF2↓, 1,   ROS∅, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,   proCasp3↑, 1,   JNK↑, 2,   MAPK↑, 1,   p27/CDKN1B↓, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,   tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   P21↓, 1,   TumCCA↑, 1,  

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

ERK↓, 1,   PI3K↓, 1,   STAT3↓, 2,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

TumVol↓, 1,  
Total Targets: 38

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: JNK, c-Jun N-terminal kinase (JNK)
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:13  Cells:%  prod#:%  Target#:168  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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