Disulfiram / SOD 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


SOD, superoxide dismutase: Click to Expand ⟱
Source:
Type:
SOD, or superoxide dismutase, is an important antioxidant enzyme that plays a crucial role in protecting cells from oxidative stress. It catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide.
SOD Isoforms: There are three main isoforms of SOD:
SOD1 (cytosolic): Often found to be overexpressed in certain tumors, which may help cancer cells survive in oxidative environments.
SOD2 (mitochondrial): Plays a critical role in protecting mitochondria from oxidative damage. Its expression can be upregulated in some cancers, contributing to tumor growth and resistance to therapy.
SOD3 (extracellular): Its role in cancer is less well understood, but it may have implications in the tumor microenvironment and metastasis.
The expression levels of SOD can serve as a prognostic indicator in some cancers. For example, high levels of SOD expression have been associated with poor prognosis in certain types of tumors, potentially due to their role in promoting tumor cell survival and resistance to therapies.
Scientific Papers found: Click to Expand⟱
4913- DSF,    Anticancer effects of disulfiram: a systematic review of in vitro, animal, and human studies
- Review, Var, NA
Apoptosis↑, tumCV↑, eff↑, toxicity↓, antiNeop↑, ChemoSen↑, RadioS↑, OS↑, ROS↑, SOD↓, MMP1↓, eff↑, Half-Life↓,
4914- DSF,  immuno,    Disulfiram and cancer immunotherapy: Advanced nano-delivery systems and potential therapeutic strategies
- Review, Var, NA
AntiTum↑, eff↑, ALDH↓, Dose↝, RadioS↑, angioG↓, TumMeta↓, BioAv↝, ROS↑, DNAdam↑, P-gp↓, CSCs↓, EMT↓, Imm↑, SOD↓, MAPK↓, NF-kB↓, ChemoSen↑, eff↑, toxicity↝, BioAv↑, *Inflam↓, Sepsis↓,

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,   SOD↓, 2,  

Cell Death ⓘ

Apoptosis↑, 1,   MAPK↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CSCs↓, 1,   EMT↓, 1,  

Migration ⓘ

MMP1↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↑, 4,   Half-Life↓, 1,   RadioS↑, 2,  

Functional Outcomes ⓘ

antiNeop↑, 1,   AntiTum↑, 1,   OS↑, 1,   toxicity↓, 1,   toxicity↝, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 28

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: SOD, superoxide dismutase
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#:298  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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