DrugR Cancer Research Results

DrugR, Drug Resistance: Click to Expand ⟱
Source:
Type:
Drug Resistance
Scientific Papers found: Click to Expand⟱
5012- DSF,  Cu,    Advancing Cancer Therapy with Copper/Disulfiram Nanomedicines and Drug Delivery Systems
ROS↑, DSF’s anticancer mechanism is primarily due to its generating reactive oxygen species, inhibiting aldehyde dehydrogenase (ALDH) activity inhibition, and decreasing the levels of transcriptional proteins
ALDH↓,
TumCP↓, DSF also shows inhibitory effects in cancer cell proliferation, the self-renewal of cancer stem cells (CSCs), angiogenesis, drug resistance, and suppresses cancer cell metastasis.
CSCs↓,
angioG↓,
TumMeta↓,
DNAdam↑, anti-cancer mechanism of DSF/Cu (II) may be mediated by the regulation of reactive oxygen species (ROS), enzyme activity regulation, induction of DNA damage, proteasome inhibition, and transcription factors
Proteasome↓,
SOD1↓, The complex of DSF and Cu (II)has been reported to inhibit the enzyme superoxide dismutase 1 (SOD1), one of the major enzymesthat mitigates oxidative damage in melanoma cells
GSR↓, The inhibition of Glutathione reductase (GSR) inhibition by DSF disrupts glutathione GSH redox cycling, producing an accumulation of oxidized glutathione (GSSG) and a lower GSH/GSSG ratio, producing an increase in ROS level
ox-GSSG↑,
GSH/GSSG↓,
MMP↓, DSF induces the disruption of the mitochondrial membrane potential and cause apoptosis in human melanoma cell lines
Akt↓, induced the apoptosis of erbB2-positive breast cancer cells by inhibiting AKT, cyclin D1, and NFκB signaling
cycD1/CCND1↓,
NF-kB↓,
CSCs↓, In hepatocellular carcinoma, DSF decreases CSCs by inhibiting the p38 mitogen-activated protein kinase (MAPK) pathway [118].
MAPK↓,
angioG↓, Thus, the inhibition of DSF/Cu (II) in CSCs decrease angiogenesis.
DrugR↓, DSF/Cu (II) overcomes drug resistance via targeting the proteasome, epithelial–mesenchymal transition (EMT), P-gp, CSC activity
EMT↓,
Vim↓, By downregulating associated proteins such as Vimentin, DSF/Cu (II) inhibits the EMT, which consequently overcomes the paclitaxel resistance of prostate and lung cancer
BioAv↑, The use of these nanoparticle-based formulations can increase the accumulation of DSF at the target site, thereby reducing the toxic effects on healthy tissues and improving the therapeutic index.
eff↑, In clinical trials, DSF is provided orally, but Cu (II) is critical for the efficacy of DSF


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 ⓘ

GSH/GSSG↓, 1,   GSR↓, 1,   ox-GSSG↑, 1,   ROS↑, 1,   SOD1↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Akt↓, 1,   MAPK↓, 1,   Proteasome↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CSCs↓, 2,   EMT↓, 1,  

Migration ⓘ

TumCP↓, 1,   TumMeta↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   DrugR↓, 1,   eff↑, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: DrugR, Drug Resistance
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

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