ROS Cancer Research Results

ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
4113- ,    ROS_levels_in_H2O2-treated_Glioblastoma_Cell_Line">Post-exposure Effects of PEMF on ROS levels in H2O2-treated Glioblastoma Cell Line
- in-vitro, Nor, U87MG
*ROS↓, *SOD2↑,
4572- ,    ROS_generation_and_uncoupling_Review">Mitochondrial electron transport chain, ROS generation and uncoupling
- Review, NA, NA
*UCPs↝, *ETC↝, *ROS↝,
4384- ,    Silver nanoparticles: synthesis, properties, and therapeutic applications
- Review, Var, NA
AntiCan↑, RadioS↑, CellMemb↑, ROS↑, DNAdam↑, PhotoS↑, eff↑,
2327- 2DG,    2-Deoxy-d-Glucose and Its Analogs: From Diagnostic to Therapeutic Agents
- Review, Var, NA
Glycolysis↓, HK2↓, mt-ROS↑, AMPK↑, PPP↓, NADPH↓, GSH↓, Bax:Bcl2↑, Apoptosis↑, RadioS↑, eff↓, Half-Life↓, other↝, eff↓,
1336- 2DG,    2-deoxy-D-glucose induces oxidative stress and cell killing in human neuroblastoma cells
- in-vitro, GBM, SK-N-SH
ROS↑, GlucoseCon↓, other↓,
1337- 2DG,  Rad,    2-deoxy-D-glucose causes cytotoxicity, oxidative stress, and radiosensitization in pancreatic cancer
- in-vivo, NA, NA
ChemoSen↑, GlucoseCon↓, ROS↑,
1339- 2DG,  Cisplatin,    2-Deoxy-d-Glucose Combined with Cisplatin Enhances Cytotoxicity via Metabolic Oxidative Stress in Human Head and Neck Cancer Cells
- in-vitro, HNSCC, FaDu
ChemoSen↑, ROS↑, GSH↓, other↓,
1341- 3BP,    The HK2 Dependent “Warburg Effect” and Mitochondrial Oxidative Phosphorylation in Cancer: Targets for Effective Therapy with 3-Bromopyruvate
- Review, NA, NA
Glycolysis↓, OXPHOS↓, *toxicity↓, ROS↑, GSH↓, eff↑,
5271- 3BP,    The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside
- Review, Var, NA
selectivity↑, selectivity↑, ATP↓, Glycolysis↓, HK2↓, mt-OXPHOS↓, GAPDH↓, mtDam↑, GSH↓, ROS↑, ER Stress↑, TumAuto↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, Akt↓, HDAC↓, TumCA↑, Bcl-2↓, cMyc↓, Casp3↑, Cyt‑c↑, Mcl-1↓, PARP↓, ChemoSen↑,
5277- 3BP,    3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model
- in-vivo, PC, Panc02
HK2↓, selectivity↑, ATP↓, mtDam↑, Dose↝, TumCG↓, Casp3↑, Glycolysis↓, NADPH↓, ATP↓, ROS↑, DNAdam↑, GSH↓, Bcl-2↓, Casp↑, lactateProd↓,
5273- 3BP,    The promising anticancer drug 3-bromopyruvate is metabolized through glutathione conjugation which affects chemoresistance and clinical practice: An evidence-based view
- Review, Var, NA
AntiCan↑, ROS↑, angioG↓, CSCs↓, Warburg↓, GSH↓, Thiols↓,
5272- 3BP,    The efficacy of the anticancer 3-bromopyruvate is potentiated by antimycin and menadione by unbalancing mitochondrial ROS production and disposal in U118 glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
Glycolysis↓, ROS↑, GPx↓, eff↓, OXPHOS↓, HK2↓, ATP↓, ROS↑, ER Stress↑, BioAv↓, Cyt‑c↑, eff↑,
5263- 3BP,  CET,    3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis
- in-vitro, CRC, DLD1 - NA, NA, HCT116
eff↑, Ferroptosis↓, TumAuto↑, Apoptosis↑, FOXO3↑, AMPKα↑, p‑Beclin-1↑, HK2↓, ATP↓, ROS↑, Dose↝, TumVol↓, TumW↓, xCT↑, GSH↓, eff↓, MDA↑,
5257- 3BP,    Tumor Energy Metabolism and Potential of 3-Bromopyruvate as an Inhibitor of Aerobic Glycolysis: Implications in Tumor Treatment
- Review, Var, NA
Glycolysis↓, mt-OXPHOS↓, HK2↓, Cyt‑c↑, Casp3↓, Bcl-2↓, Mcl-1↓, GAPDH↓, LDH↓, PDH↓, TCA↓, GlutaM↓, GSH↓, ATP↓, mitResp↓, ROS↑, ChemoSen↑, toxicity↝,
5270- 5-ALA,  PDT,    5-Aminolevulinic Acid as a Theranostic Agent for Tumor Fluorescence Imaging and Photodynamic Therapy
- Review, Var, NA
other↝, ROS↑, other↝, mtDam↑, Ca+2↑, ER Stress↑, Apoptosis↑, TumAuto↑, other↝, Dose↝, Imm↑,
3453- 5-ALA,    The heme precursor 5-aminolevulinic acid disrupts the Warburg effect in tumor cells and induces caspase-dependent apoptosis
- in-vitro, Lung, A549
OXPHOS↑, OCR↑, Warburg↓, ROS↑, SOD2↑, Catalase↑, HO-1↑, Casp3↑, Apoptosis↑,
4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, TumCCA↑, Apoptosis↑, eff↑, Bcl-2↓, survivin↓, P21↑, p27↑, BAX↑, Cyt‑c↑, Casp3↑, PI3K↓, Akt↓, mTOR↓, Hif1a↓, PTEN↑, AMPKα↑, PDH↑, LDHA↓, antiOx↓, ROS↑, AntiCan↑,
5296- 5-HTP,    Serotonergic Regulation in Alzheimer’s Disease
- Review, AD, NA
*Risk↓, *5HT↓, *ROS↓, *MDA↓, *Apoptosis↓, *Mood↑, *other↑, *other↑,
5289- 5-HTP,    5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology
- Review, AD, NA - Review, Arthritis, NA
*5HT↑, *Inflam↓, *memory↑, *Sleep↑, *Weight↓, *DNAdam↓, *ROS↓, *toxicity↝,
3970- ACNs,    Anthocyanin-rich blueberry extracts and anthocyanin metabolite protocatechuic acid promote autophagy-lysosomal pathway and alleviate neurons damage in in vivo and in vitro models of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, *LDH↓, *ROS↓, *neuroP↑,
3969- ACNs,    Blueberry Supplementation in Midlife for Dementia Risk Reduction
- Human, AD, NA
*memory↑, *cognitive↑, *ROS↓,
3864- ACNs,    Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, *Aβ↓, *ROS↓, *cognitive↑, *APP↓, *BBB↑, *Ca+2↓, *ATP↑, *BACE↓, *p‑NF-kB↓, *TNF-α↓, *iNOS↓,
5459- AF,    Auranofin Induces Lethality Driven by Reactive Oxygen Species in High-Grade Serous Ovarian Cancer Cells
- in-vitro, Ovarian, NA
ROS↑, TrxR↓, MMP↓, Apoptosis↑, eff↓, Casp3↑, Casp7↑, DNAdam↑, eff↑, GSH↓, angioG↓, ChemoSen↑, cl‑PARP↑, eff↑,
5466- AF,    Auranofin Inhibition of Thioredoxin Reductase in a Preclinical Model of Small Cell Lung Cancer
- in-vivo, Lung, NA
TrxR↓, Dose↝, RadioS↑, ChemoSen↑, ROS↑, Diff↑, toxicity↓,
5465- AF,    The Thioredoxin Reductase Inhibitor Auranofin Suppresses Pulmonary Metastasis of Osteosarcoma, But Not Local Progression
- in-vitro, OS, NA
TrxR↓, ROS↑, TumCMig↓,
5464- AF,    Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies
- vitro+vivo, GBM, NA
TrxR↓, BioAv↓, ROS↑, eff↝, TET1?, BioAv↑,
5463- AF,    Will Auranofin Become a Golden New Treatment Against COVID-19?
- Review, Covid, NA
IL6↓, NF-kB↓, ATF2↓, TrxR↓, ROS↑, Apoptosis↑, IL6↓, Dose↑,
5462- AF,    Repurposing Auranofin for Oncology and Beyond: A Brief Overview of Clinical Trials as Mono- and Combination Therapy
- Review, Var, NA
AntiTum↑, Bacteria↓, TrxR↓, ChemoSen↑, Dose↝, ROS↑, Apoptosis↑, mTOR↓,
5461- AF,    Dual inhibition of thioredoxin reductase and proteasome is required for auranofin-induced paraptosis in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
Paraptosis↑, ER Stress↑, TrxR↓, selectivity↑, toxicity↝, ROS↑, mt-TrxR1↓, mt-TrxR2↓,
5460- AF,    Auranofin radiosensitizes tumor cells through targeting thioredoxin reductase and resulting overproduction of reactive oxygen species
- vitro+vivo, Var, 4T1
RadioS↑, ROS↑, eff↓, mt-OCR↓, DNAdam↑, Apoptosis↑, TrxR↓, eff↑,
5472- AF,    Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion
- in-vitro, Cerv, HeLa
TrxR↓, AntiCan↑, TumCG↓, Apoptosis↑, necrosis↑, cl‑PARP↑, MMP↓, ROS↑, GSH↓, eff↓,
5471- AF,    Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice
- vitro+vivo, Melanoma, B16-F10
TrxR1↓, AntiTum↑, ROS↑, NRF2↑, TumCD↑,
5470- AF,    Exploring a Therapeutic Gold Mine: The Antifungal Potential of the Gold-Based Antirheumatic Drug Auranofin
- Review, Var, NA
TrxR↓, other↝, IL6↑, IL8↑, NK cell⇅, COX2↓, NOS2↓, NRF2↑, Prx↑, Half-Life↑, Dose↝, ROS↑, NF-kB↓,
5468- AF,    The gold complex auranofin: new perspectives for cancer therapy
- Review, Var, NA
TrxR↓, ROS↑, eff↑, Apoptosis↑, TumCG↓, TumCP↓, Akt↓, NF-kB↓, DNAdam↑, eff↝, eff↓, PI3K↓, Akt↓, mTOR↓, Hif1a↓, VEGF↓, Casp3↑, CSCs↓, ATP↓, Glycolysis↓, eff↑, eff↑, MMP↓, AIF↑, toxicity↓,
1900- AF,    Potential Anticancer Activity of Auranofin
- Review, Var, NA
TrxR↓, ROS↑, Apoptosis↓, TumCP↓, eff↑,
5430- AG,    Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation
- Review, Stroke, NA
*cardioP↑, *MitoP↑, *ROS↓, *mtDam↓, *neuroP↓, TumAuto↓, *AntiDiabetic↑,
5434- AG,    Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview
- Review, Liver, NA
AntiCan↑, Apoptosis↑, TumCP↓, EMT↓, Imm↑, ChemoSen↑, BioAv↓, TumCG↓, IL2↑, IL12↑, TNF-α↑, P-gp↓, MDR1↓, QoL↑, Casp↑, DNAdam↑, Bcl-2↓, BAX↑, MMP↓, Cyt‑c↑, NOTCH1↓, GSK‐3β↓, TumCCA↑, GSH↓, ROS↑, lipid-P↑, c-Iron↑, GPx4↓, ACSL4↑, Ferroptosis↑, Wnt↓, β-catenin/ZEB1↓, cycD1/CCND1↓, Akt↓, PI3K↓, mTOR↓, CXCR4↓, Vim↓, PD-L1↓, eff↑, eff↑, ChemoSen↑, ChemoSen↑, chemoP↑,
5236- AgNPs,    Adaptive regulations of Nrf2 alleviates silver nanoparticles-induced oxidative stress-related liver cells injury
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
tumCV↓, ROS↑, *ROS↑, DNAdam↑, *DNAdam↑, eff↓, selectivity↑,
5238- AgNPs,    β-Sitosterol-assisted silver nanoparticles activates Nrf2 and triggers mitochondrial apoptosis via oxidative stress in human hepatocellular cancer cell line
- in-vitro, HCC, HepG2
TumCP↓, ROS↑, NRF2↑, BAX↑, P53↑, Cyt‑c↑, Casp9↑, Casp3↑, Bcl-2↓,
5239- AgNPs,    NOX4- and Nrf2-mediated oxidative stress induced by silver nanoparticles in vascular endothelial cells
- in-vitro, Nor, HUVECs
*ROS↑, *Apoptosis↑, *NRF2↝,
1406- AgNPs,    The antioxidant effects of silver, gold, and zinc oxide nanoparticles on male mice in in vivo condition
- in-vivo, Nor, NA
*ROS↓, *GPx↑, *Catalase↑, *ROS↑,
1908- AgNPs,    Exposure to Silver Nanoparticles Inhibits Selenoprotein Synthesis and the Activity of Thioredoxin Reductase
- in-vitro, Lung, A549
TrxR↓, TrxR1↓, ROS↑, ER Stress↑, TumCP↓, selenoP↓,
1905- AgNPs,    Evaluation of the effect of silver and silver nanoparticles on the function of selenoproteins using an in-vitro model of the fish intestine: The cell line RTgutGC
- in-vivo, Nor, NA
*TrxR↓, *ROS∅, GPx↑,
1903- AgNPs,    Novel Silver Complexes Based on Phosphanes and Ester Derivatives of Bis(pyrazol-1-yl)acetate Ligands Targeting TrxR: New Promising Chemotherapeutic Tools Relevant to SCLC Managemen
- in-vitro, Lung, U1285
TrxR↓, eff↝, ROS↑,
4403- AgNPs,    Silver Nanoparticles Decorated UiO-66-NH2 Metal-Organic Framework for Combination Therapy in Cancer Treatment
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vitro, GBM, GL26 - in-vitro, Cerv, HeLa - in-vitro, CRC, RKO
AntiCan↑, eff↑, EPR↑, selectivity↑, ROS↑, Casp↑, Apoptosis↑, DNAdam↑, tumCV↓, eff↑,
4404- AgNPs,  Rad,    Main Approaches to Enhance Radiosensitization in Cancer Cells by Nanoparticles: A Systematic Review
- Review, Var, NA
eff↑, ROS↑,
4400- AgNPs,  Rad,    Differential cytotoxic and radiosensitizing effects of silver nanoparticles on triple-negative breast cancer and non-triple-negative breast cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, MDA-MB-231
ROS↑, DNAdam↑, selectivity↑, TumCG↓, RadioS↑, Dose↝, selectivity↑, other↝, eff↓, eff↑, γH2AX↑, Dose↓, eff↑,
4399- AgNPs,  Chit,    Silver nanoparticles impregnated alginate-chitosan-blended nanocarrier induces apoptosis in human glioblastoma cells
- in-vitro, GBM, U87MG
DNAdam↑, ROS↑, MMP↓, eff↑,
4398- AgNPs,    Induction of apoptosis in cancer cells at low silver nanoparticle concentrations using chitosan nanocarrier
- in-vitro, Colon, HT29
Apoptosis↑, MMP↓, Casp3↑, ROS↑, eff↑,
4389- AgNPs,    Graphene Oxide-Silver Nanocomposite Enhances Cytotoxic and Apoptotic Potential of Salinomycin in Human Ovarian Cancer Stem Cells (OvCSCs): A Novel Approach for Cancer Therapy
- in-vitro, Ovarian, NA
tumCV↓, ROS↑, LDH↓, MMP↑, CSCs↓, AntiCan↑,

Showing Research Papers: 1 to 50 of 2062
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2062

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   MDA↓, 1,   NRF2↝, 1,   ROS↓, 8,   ROS↑, 3,   ROS↝, 1,   ROS∅, 1,   SOD2↑, 1,   TrxR↓, 1,   UCPs↝, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   ETC↝, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Apoptosis↑, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 2,  

Autophagy & Lysosomes ⓘ

MitoP↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   DNAdam↑, 1,  

Migration ⓘ

APP↓, 1,   Ca+2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   p‑NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,   5HT↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Clinical Biomarkers ⓘ

LDH↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   cognitive↑, 3,   memory↑, 2,   Mood↑, 1,   neuroP↓, 1,   neuroP↑, 1,   Risk↓, 1,   Sleep↑, 1,   toxicity↓, 1,   toxicity↝, 1,   Weight↓, 1,  
Total Targets: 46

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
117 Silver-NanoParticles
91 Quercetin
88 Magnetic Fields
78 Curcumin
74 Thymoquinone
55 Shikonin
53 Vitamin C (Ascorbic Acid)
49 Berberine
49 Sulforaphane (mainly Broccoli)
48 Resveratrol
47 Lycopene
43 Radiotherapy/Radiation
43 Baicalein
42 Alpha-Lipoic-Acid
40 Selenite (Sodium)
40 Ashwagandha(Withaferin A)
40 Piperlongumine
38 Artemisinin
37 Betulinic acid
36 EGCG (Epigallocatechin Gallate)
36 Hydrogen Gas
33 Rosmarinic acid
32 Silymarin (Milk Thistle) silibinin
29 Propolis -bee glue
29 Fisetin
29 Selenium NanoParticles
28 Apigenin (mainly Parsley)
27 Honokiol
26 Allicin (mainly Garlic)
25 Chemotherapy
25 Phenethyl isothiocyanate
24 Luteolin
24 Magnetic Field Rotating
23 Copper and Cu NanoParticles
22 Vitamin K2
21 doxorubicin
21 Gambogic Acid
20 Juglone
18 Cisplatin
18 Chrysin
17 Boron
17 salinomycin
17 Parthenolide
16 Urolithin
15 Coenzyme Q10
14 Auranofin
14 Boswellia (frankincense)
14 Capsaicin
14 Phenylbutyrate
13 chitosan
13 Selenium
13 Ellagic acid
13 Emodin
13 Pterostilbene
12 Photodynamic Therapy
12 Caffeic acid
12 VitK3,menadione
11 5-fluorouracil
11 Astaxanthin
11 Dichloroacetate
11 Graviola
11 Piperine
10 Melatonin
10 Ursolic acid
10 diet FMD Fasting Mimicking Diet
10 Ferulic acid
10 Plumbagin
9 SonoDynamic Therapy UltraSound
9 Andrographis
9 Bacopa monnieri
9 borneol
8 Electrical Pulses
8 Sulfasalazine
8 Hyperthermia
8 Methylene blue
8 Moringa oleifera
8 Propyl gallate
7 3-bromopyruvate
7 Gold NanoParticles
7 Metformin
7 Berbamine
7 brusatol
7 Carnosine
7 Hydroxycinnamic-acid
7 diet Methionine-Restricted Diet
7 Disulfiram
7 HydroxyTyrosol
6 2-DeoxyGlucose
6 Gemcitabine (Gemzar)
6 immunotherapy
6 Biochanin A
6 Butyrate
6 Citric Acid
6 Aflavin-3,3′-digallate
6 Nimbolide
5 Brucea javanica
5 Bromelain
5 erastin
5 Spermidine
5 Crocetin
5 Huperzine A/Huperzia serrata
5 Garcinol
5 HydroxyCitric Acid
5 Magnolol
5 nicotinamide adenine dinucleotide
5 Rutin
4 Docetaxel
4 Carnosic acid
4 Vitamin E
4 diet Short Term Fasting
4 γ-linolenic acid (Borage Oil)
4 Magnesium
4 Naringin
4 Taurine
3 5-Aminolevulinic acid
3 Anthocyanins
3 Glucose
3 Zinc
3 temozolomide
3 Black phosphorus
3 Paclitaxel
3 Cinnamon
3 Date Fruit Extract
3 Oxygen, Hyperbaric
3 Shilajit/Fulvic Acid
3 Ginkgo biloba
3 Orlistat
3 MCToil
3 Methylsulfonylmethane
3 Mushroom Lion’s Mane
3 Oleuropein
3 EMF
3 Shankhpushpi
3 Vitamin B1/Thiamine
2 5-Hydroxytryptophan
2 Astragalus
2 Aromatherapy
2 Ascorbyl Palmitate
2 Atorvastatin
2 Aloe anthraquinones
2 beta-glucans
2 Baicalin
2 beta-carotene(VitA)
2 Bufalin/Huachansu
2 Bruteridin(bergamot juice)
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Catechins
2 Calorie Restriction Mimetics
2 Galantamine
2 Folic Acid, Vit B9
2 Fenbendazole
2 Galloflavin
2 Potassium
2 Methyl Jasmonate
2 Methylglyoxal
2 Myricetin
2 Vitamin B3,Niacin
2 Niclosamide (Niclocide)
2 Pachymic acid
2 Sanguinarine
2 Psoralidin
2 Radio Frequency
2 Sesame seeds and Oil
2 Iron
2 Salvia miltiorrhiza
2 Vitamin D3
1 cetuximab
1 Anzaroot, Astragalus fasciculifolius Bioss
1 entinostat
1 Camptothecin
1 Resiquimod
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 alpha Linolenic acid
1 Anti-oxidants
1 Sorafenib (brand name Nexavar)
1 tamoxifen
1 almonertinib
1 D-limonene
1 epirubicin
1 Lapatinib
1 Ras-selective lethal 3
1 Chlorogenic acid
1 Cannabidiol
1 Celastrol
1 Choline
1 Aspirin -acetylsalicylic acid
1 chemodynamic therapy
1 methylseleninic acid
1 Rivastigmine
1 Docosahexaenoic Acid
1 diet Ketogenic
1 diet Plant based
1 Exercise
1 Fucoidan
1 Gallic acid
1 verapamil
1 hydroxychloroquine
1 Ginseng
1 hydrogen sulfide
1 Rapamycin
1 Ivermectin
1 lambertianic acid
1 Myrrh
1 N-Acetyl-Cysteine
1 Oleocanthal
1 sericin
1 Kaempferol
1 benzo(a)pyrene
1 Hyperoside
1 Perilla
1 Salvia officinalis
1 Oxaliplatin
1 Scoulerine
1 polyethylene glycol
1 acetaminophen
1 Formononetin
1 Silicic Acid
1 Squalene
1 Osimertinib
1 Adagrasib
1 Glutathione
1 statins
1 Safflower yellow
1 triptolide
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B2,Riboflavin
1 Vitamin B5,Pantothenic Acid
1 glucose deprivation
1 Transarterial Chemoembolization
1 probiotics
1 xanthohumol
1 Zinc Oxide
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#:%  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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