Disulfiram / MMP1 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


MMP1, Matrix metalloproteinases: Click to Expand ⟱
Source:
Type:
MMP-1, or matrix metalloproteinase-1, is an enzyme that plays a significant role in the degradation of extracellular matrix components, particularly collagen. It is part of a larger family of matrix metalloproteinases (MMPs) that are involved in various physiological and pathological processes, including tissue remodeling, wound healing, and inflammation.
MMP-1 facilitates the breakdown of the extracellular matrix, which can promote tumor invasion into surrounding tissues and the spread of cancer cells to distant sites (metastasis). By degrading collagen and other matrix components, MMP-1 can help create pathways for cancer cells to migrate. Elevated levels of MMP-1 have been associated with poor prognosis in various types of cancer, including breast, lung, and colorectal cancers.
- In many cancers, high MMP-1 expression levels have been correlated with poor prognosis, indicating that it may serve as a potential biomarker for assessing tumor aggressiveness and patient outcomes.
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↓,

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 ⓘ

ROS↑, 1,   SOD↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Migration ⓘ

MMP1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 2,   Half-Life↓, 1,   RadioS↑, 1,  

Functional Outcomes ⓘ

antiNeop↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MMP1, Matrix metalloproteinases
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#:198  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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