HNE Cancer Research Results

HNE, 4-hydroxynonenal (HNE): Click to Expand ⟱
Source:
Type:
HNE is a lipid peroxidation product formed during oxidative stress and is considered both a signaling molecule and a cytotoxic agent depending on its cellular concentration and context.
– HNE is generated as a byproduct of the peroxidation of ω-6 polyunsaturated fatty acids.
– It serves as a marker of oxidative stress and can modify proteins, lipids, and DNA through covalent adduct formation.

• Dual Biological Effects
– At low to moderate concentrations, HNE can act as a signaling molecule, modulating pathways involved in cell proliferation, differentiation, and apoptosis.
– At higher concentrations, HNE is cytotoxic, causing cellular damage and contributing to cell death through protein dysfunction and DNA damage.
– This concentration-dependent activity means that HNE can have both pro-tumorigenic and anti-tumorigenic effects.

– Elevated levels of HNE in tissues or biological fluids are frequently used as indicators of oxidative stress within the tumor microenvironment.
Scientific Papers found: Click to Expand⟱
1571- Cu,    Copper in cancer: From pathogenesis to therapy
- Review, NA, NA
*toxicity↝, The toxicity of Cu overload is known to be due, in part, to the release of ROS via the Fenton or Haber-Weiss reaction, causing lipid, protein, DNA, and RNA damage
ROS↑, Cu-induced ROS can induce lipid peroxidation, which raises hydroxynonenal (HNE) levels and causes lipid peroxidation to become toxic.
lipid-P↓,
HNE↑, raises hydroxynonenal (HNE) levels and causes lipid peroxidation to become toxic
MAPK↑, Cu exposure causes an elevation in intracellular ROS levels, which then stimulates the MAPK signaling pathway, increasing JNK/SAPK and p38 homologous activity and phosphorylation levels
JNK↑, Cu-induced ROS continuously activate JNK, promote the production of the AP-1 transcription factor, increase Beclin 1 and Atg7 production, and cause autophagy and apoptosis in tumor cells
AP-1↑,
Beclin-1↑,
ATG7↑,
TumAuto↑,
Apoptosis↑,
HO-1↑, Fang and colleagues consistently found that Cu activates the ROS/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase-1 (NQO1) signaling cascade to induce autophagy
NQO1↑,
mt-ROS↑, Cu NPs induce complete autophagy by enhancing mitochondrial ROS production and inducing autophagy
Fenton↑, generating large amounts of ROS and oxygen via a Fenton-like reaction


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   HNE↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   NQO1↑, 1,   ROS↑, 1,   mt-ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

ATG7↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   JNK↑, 1,   MAPK↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 1,  

Migration ⓘ

AP-1↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↝, 1,  
Total Targets: 1

Scientific Paper Hit Count for: HNE, 4-hydroxynonenal (HNE)
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:%  Cells:%  prod#:%  Target#:1137  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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