DrugR Cancer Research Results
DrugR, Drug Resistance: Click to Expand ⟱
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| Type: |
Drug Resistance
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Scientific Papers found: Click to Expand⟱
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
TumCG↓, Nimbolide, the most potent cytotoxic neem limonoid, inhibits the growth of cancer cells by regulating the phosphorylation of keystone kinases that drive oncogenic signaling besides modulating the epigenome.
TumCP↓, preventing the acquisition of hallmark traits of cancer, such as cell proliferation, apoptosis evasion, inflammation, invasion, angiogenesis, and drug resistance.
Apoptosis↑,
Inflam↓,
angioG↓,
DrugR↓,
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(tgid=1) ⓘ
GSH/GSSG↓, 1, GSR↓, 1, ox-GSSG↑, 1, ROS↑, 1, SOD1↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 1, MAPK↓, 1, Proteasome↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
cycD1/CCND1↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ALDH↓, 1, CSCs↓, 2, EMT↓, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
TumCP↓, 2, TumMeta↓, 1, Vim↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 1, NF-kB↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, DrugR↓, 2, eff↑, 1,
Total Targets: 25
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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