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.
PC, Pancreatic Cancer: Click to Expand ⟱
Pancreatic Cancer: Hypoxia (low oxygen tension) is commonly found in solid tumors. Hypoxia-inducible factor-1 (HIF-1),is a key mediator of the cellular response to hypoxia and is overexpressed in a wide variety of solid tumors, including pancreatic cancer.
Nanog is highly expressed in CSCs compared to normal cells [93–97]
HIF-1↑
Scientific Papers found: Click to Expand⟱
5836- CAP,    In vitro and in vivo induction of apoptosis by capsaicin in pancreatic cancer cells is mediated through ROS generation and mitochondrial death pathway
- vitro+vivo, PC, AsPC-1 - in-vitro, PC, Bxpc-3
tumCV↓, Apoptosis↑, ROS↑, MMP↓, eff↓, BAX↑, Bcl-2↓, survivin↓, Cyt‑c↑, AIF↑, selectivity↑, JNK↑, TumCG↓,
1674- PBG,  SDT,  HPT,    Study on the effect of a triple cancer treatment of propolis, thermal cycling-hyperthermia, and low-intensity ultrasound on PANC-1 cells
- in-vitro, PC, PANC1 - in-vitro, Nor, H6c7
tumCV↓, ROS↑, eff↑, Dose∅, selectivity↑, MMP↓, mtDam↑, cl‑PARP↑, p‑ERK↓, p‑JNK↑, p‑p38↑, eff↓, ChemoSen↑,

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 ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 2,   mtDam↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Cyt‑c↑, 1,   JNK↑, 1,   p‑JNK↑, 1,   p‑p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,   TumCG↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 1,   selectivity↑, 2,  
Total Targets: 21

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:21  Cells:%  prod#:%  Target#:168  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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