Disulfiram / ATF2 Cancer Research Results

DSF, Disulfiram: Click to Expand ⟱
Features:
Disulfiram is a synthetic small-molecule drug best known for its use in the treatment of chronic alcohol use disorder. It is a thiuram disulfide compound with the chemical formula C₁₀H₂₀N₂S₄ and acts primarily as an aldehyde dehydrogenase (ALDH) inhibitor. 
Main Actions:
-Potent copper-dependent pro-oxidant
-Targets ALDH⁺ cancer stem cells
-Strong clinical repurposing interest

Key pathways
-Cu-mediated redox cycling
-Proteasome inhibition
-Mitochondrial ROS

Chemo relevance
-Often synergistic
-Highly mechanism-dependent
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Metal chelation / Disulfiram–Cu complex formation ↑ DSF–Cu complex formation ↔ limited formation Driver Copper-dependent cytotoxic chemistry Elevated copper in cancer cells enables formation of cytotoxic DSF–Cu complexes; this is the initiating event for most anticancer effects
2 Proteasome / p97–NPL4 axis ↓ proteasome function; ↑ proteotoxic stress ↔ minimal disruption Driver Protein homeostasis collapse DSF–Cu disrupts protein degradation pathways, leading to accumulation of misfolded proteins and stress signaling
3 Reactive oxygen species (ROS) ↑ ROS (metal-dependent) ↔ buffered Secondary Oxidative stress amplification ROS rise follows DSF–Cu redox cycling and proteotoxic stress; not the primary trigger
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Secondary Execution of cell death Mitochondrial dysfunction and apoptosis occur downstream of proteostasis and redox stress
5 ALDH activity (ALDH1A1 / stemness) ↓ ALDH activity ↓ ALDH (clinically tolerated) Secondary Cancer stem-like cell targeting ALDH inhibition preferentially impacts cancer stem-like populations; normal cells tolerate inhibition at therapeutic exposure
6 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of survival transcription NF-κB inhibition reflects upstream proteotoxic and redox stress rather than direct targeting
7 Cell cycle progression ↓ proliferation / ↑ arrest ↔ largely spared Phenotypic Cytostatic growth control Growth inhibition reflects impaired protein turnover and metabolic stress
8 Apoptosis / non-apoptotic death ↑ apoptosis or proteotoxic death ↔ protected Phenotypic Threshold-dependent cell death Cell death modality depends on copper availability and stress magnitude


ATF2, Activating Transcription Factor 2: Click to Expand ⟱
Source:
Type:
ATF2 (Activating Transcription Factor 2)
-ATF2 is a member of the ATF/CREB (cyclic AMP response element‐binding protein) family of transcription factors.
-It functions by binding to specific DNA sequences to regulate the transcription of a variety of target genes involved in cell proliferation, stress response, apoptosis, and differentiation.
-ATF2 activity is regulated through phosphorylation by stress-activated protein kinases such as JNK, p38, and ERK, integrating signals from various cellular stressors.

-Increased ATF2 activity in certain lung cancer subtypes has been linked with increased invasiveness and metastatic potential.
Scientific Papers found: Click to Expand⟱
5013- DSF,  Cu,  Z,    Disulfiram inhibits activating transcription factor/cyclic AMP-responsive element binding protein and human melanoma growth in a metal-dependent manner in vitro, in mice and in a patient with metastatic disease
- vitro+vivo, Melanoma, NA - Case Report, Melanoma, NA
P-gp↓, NF-kB↓, ChemoSen↑, angioG↓, TumCG↓, TumMeta↓, Remission↑, toxicity↓, ATF2↓, CREB↓, cycA1/CCNA1↓, TumCG↓, angioG↓, Dose↝, toxicity↝,

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:


Core Metabolism/Glycolysis ⓘ

CREB↓, 1,  

Cell Death ⓘ

ATF2↓, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 2,  

Migration ⓘ

TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,  

Functional Outcomes ⓘ

Remission↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ATF2, Activating Transcription Factor 2
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#:387  Target#:1295  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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