Silver-NanoParticles / ROS Cancer Research Results

AgNPs, Silver-NanoParticles: Click to Expand ⟱
Features:
Silver NanoParticles (AgNPs)
Summary:
1.Smaller sizes are generally more bioactive due to increased surface area and enhanced tumor accumulation via the enhanced permeability and retention (EPR) effect.
2.Two relevant forms: particulate silver (AgNPs) and ionic silver (Ag⁺). There is debate regarding oral use, as Ag⁺ can precipitate as AgCl in gastric acid, reducing bioavailability; AgNPs may partially avoid this via particulate uptake and intracellular Ag⁺ release. Gastric pH may influence this equilibrium.
3. Dose example 80kg person: 1.12-2mg/day, which can be calculated based on ppm and volume taken (see below) target < 10ppm and 120mL per day (30ppm and 1L per day caused argyria 30mg/day ) (Case Report: 9‐15 ppm@120mL, i.e. 1.1mg/L to 1.8mg/L per day)
Likely 10ppm --> 10mg/L, hence if take 100mL, then 1mg/day? (for Cancer)
The current Rfd for oral silver exposure is 5 ug/kg/d with a critical dose estimated at 14 ug/kg/d for the average person.
Seems like the Cancer target range is 14ug/kg/day to 25ug/kg/day. 80Kg example: 1.12mg to 2mg “1.4µg/kg body weight. If I would have 70kg, I would want to use 100µg/day. However, for fighting active disease, I would tend to explore higher daily dose, as I think this may be too low.”
These values reflect experimental or anecdotal contexts and are not established safe or therapeutic doses.
4. Antioxidants such as NAC can counteract AgNP cytotoxicity by restoring glutathione pools and suppressing ROS-mediated mitochondrial damage.
5. In vitro studies commonly show ROS elevation in both cancer and normal cells; however, in vivo, superior antioxidant, NRF2, and repair capacity in normal tissues may confer selectivity.
6. Pathways/mechanisms of action/:
-” intracellular ROS was increased...reduction in levels of glutathione (GSH)”
- Normal-cell selectivity is partly mediated by NRF2-dependent antioxidant and detoxification responses.
- AgNPs impair mitochondrial electron transport, increasing electron leak and amplifying ROS upstream of ΔΨm collapse.
-AgNPs inhibit VEGF-driven endothelial signaling and permeability (anti-angiogenic effect)
-”upregulation of proapoptotic genes (p53, p21, Bax, and caspases) and downregulation of antiapoptotic genes (Bcl-2)”
-” upregulation of AMPK and downregulation of mTOR, MMP-9, BCL-2, and α-SMA”
-”p53 is a key player...proapoptotic genes p53 and Bax were significantly increased... noticeable reduction in Bcl-2 transcript levels”
-” p53 participates directly in the intrinsic apoptosis pathway by regulating the mitochondrial outer membrane permeabilization”
- “Proapoptotic markers (BAX/BCL-XL, cleaved poly(ADP-ribose) polymerase, p53, p21, and caspases 3, 8 and 9) increased.”
-”The antiapoptotic markers, AKT and NF-kB, decreased in AgNP-treated cells.”

Chronic accumulation and long-term systemic effects remain insufficiently characterized.

Silver NanoParticles and Magnetic Fields
Summary:
1. “exposure to PMF increased the ability of AgNPs uptake”
2. 6x improvement from AgNPs alone

could glucose capping of SilverNPs work as trojan horse?

Sodium selenite might protect against toxicity of AgNPs in normal cells.

-uncoated AgNPs can degrade the gut microbiome. PVP, citrate, green-synthesized, chitosan coating, may reduce the effect.
Similar oxidative considerations may apply to selenium compounds, though mechanisms differ.
co-ingestion with food (higher pH) favors reduction and lower Ag+ levels.
-action mechanisms of AgNPs: the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.

AgNP anticancer effects come from three overlapping mechanisms:
-Nanoparticle–cell interaction (uptake, membrane effects)
-Intracellular ROS generation
-Controlled Ag⁺ release inside cancer cells

Comparison adding Citrate Capping
| Property              | Uncapped AgNPs | Citrate-capped AgNPs |
| --------------------- | -------------- | -------------------- |
| Stability             | Poor           | Excellent            |
| Free Ag⁺              | High           | Low                  |
| Normal cell toxicity  | Higher         | Lower                |
| Cancer selectivity    | Lower          | **Higher**           |
| Mechanism specificity | Crude          | **Targeted**         |
| Storage behavior      | Degrades       | Stable               |

Rank Pathway / Target Axis Cancer Cells Normal Cells Primary Effect Notes / Cancer Relevance Ref
1 Oxidative stress / ROS generation ↑ ROS (sustained) ↑ transient ROS → ↓ net ROS after adaptation Upstream cytotoxic trigger AgNP exposure commonly elevates ROS in cancer cells, initiating downstream stress-death programs (ref)
2 Thiol buffering (GSH pool) ↓ GSH (depletion) ↔ or transient ↓ with recovery Loss of redox buffering Colon cancer model: AgNPs induce oxidative cell damage through inhibition/depletion of reduced glutathione with downstream mitochondrial apoptosis (ref)
3 Mitochondrial ETC / respiration ↓ ETC efficiency; ↑ electron leak ↔ mild inhibition with recovery Bioenergetic destabilization ETC impairment amplifies ROS, precedes ΔΨm loss, and contributes to ATP collapse in cancer cells
4 Mitochondrial integrity (ΔΨm / MMP) ↓ ΔΨm ↔ largely preserved Mitochondrial dysfunction Breast cancer model: AgNP exposure dissipates mitochondrial membrane potential during cytotoxic progression (ref)
5 Intrinsic apoptosis (caspase cascade) ↑ caspase-dependent apoptosis ↔ minimal activation Programmed cell death Colon cancer model: “silver-based nanoparticles” induce apoptosis mediated through p53 (apoptosis direction shown) (ref)
6 Genotoxic stress / DNA damage ↑ DNA damage ↑ damage at high dose with efficient repair Checkpoint/death signaling Study documents AgNP-mediated DNA damage; susceptibility increases with impaired DNA repair capacity (ref)
7 ER stress / UPR (CHOP-dependent) ↑ ER stress → apoptosis ↑ adaptive UPR (no CHOP) Proteotoxic stress signaling Breast cancer cells: AgNPs induce “irremediable” ER stress leading to UPR-dependent apoptosis (ref)
8 Autophagy program ↑ autophagy (protective) ↑ adaptive autophagy Stress adaptation AgNPs induce autophagy in cancer cells; inhibiting autophagy enhances AgNP anticancer killing (ref)
9 Autophagic flux / lysosomal function ↓ flux (lysosomal defect) ↔ preserved flux Autophagic failure AgNP-induced lysosomal dysfunction drives autophagic flux defects (LC3-II accumulation) (ref)
10 NRF2 antioxidant response ↔ insufficient activation ↑ NRF2 activation Adaptive redox defense NRF2 activation in normal cells restores GSH and antioxidant enzymes, limiting toxicity
11 Stress MAPK (p38) / checkpoint signaling ↑ p38 → arrest/apoptosis ↑ transient p38 → recovery Stress signaling Jurkat T-cell model shows p38 MAPK activation with DNA damage and apoptosis (ref)
12 Angiogenesis / invasion (VEGF, NF-κB-linked) ↓ angiogenesis / ↓ invasion ↔ minimal effect Anti-angiogenic / anti-invasive AgNPs inhibit VEGF-induced permeability and invasion in tumor models (ref)


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⟱
4584- AgNPs,    Silver Nanoparticles Synthesized Using Carica papaya Leaf Extract (AgNPs-PLE) Causes Cell Cycle Arrest and Apoptosis in Human Prostate (DU145) Cancer Cells
- in-vitro, Pca, DU145
selectivity↑, ROS↑, BAX↑, cl‑Casp3↑, p‑PARP↑, TumCCA↑, cycD1/CCND1↓, p27↑, P21↑, AntiCan↑,
4583- AgNPs,    Metal-Based Nanoparticles for Cardiovascular Diseases
- Review, NA, NA
RadioS↑, *ROS↑, *BBB↝,
4564- AgNPs,  GoldNP,  Cu,  Chemo,  PDT  Cytotoxicity and targeted drug delivery of green synthesized metallic nanoparticles against oral Cancer: A review
- Review, Var, NA
ROS↑, DNAdam↑, TumCCA↑, eff↑, Apoptosis↑, eff↓, ChemoSen↑,
4563- AgNPs,  Rad,    Silver nanoparticles enhance neutron radiation sensitivity in cancer cells: An in vitro study
- in-vitro, BC, MCF-7 - in-vitro, Ovarian, SKOV3 - in-vitro, GBM, U87MG - in-vitro, Melanoma, A431
RadioS↑, ROS↑, TumCCA↑, Apoptosis↑, ER Stress↑,
4561- AgNPs,  VitC,    Cellular Effects Nanosilver on Cancer and Non-cancer Cells: Potential Environmental and Human Health Impacts
- in-vitro, CRC, HCT116 - in-vitro, Nor, HEK293
NRF2↑, TumCCA↑, ROS↑, selectivity↑, *AntiViral↑, *toxicity↝, ETC↓, MMP↓, DNAdam↑, Apoptosis↑, lipid-P↑, other↝, UPR↑, *GRP78/BiP↑, *p‑PERK↑, *cl‑eIF2α↑, *CHOP↑, *JNK↑, Hif1a↓, AntiCan↑, *toxicity↓, eff↑,
4559- AgNPs,    Anticancer activity of biogenerated silver nanoparticles: an integrated proteomic investigation
- in-vitro, BC, SkBr3 - in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, Colon, Caco-2
MMP2↓, MMP9↓, ROS↑, TumAuto↑, Apoptosis↑, ER Stress↑,
4558- AgNPs,    Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells
- in-vitro, PC, PANC1
ROS↑, selectivity↑, NO↑, SOD↓, GPx4↓, Catalase↓, TumCCA↑, MMP↓,
4557- AgNPs,    The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells
- in-vitro, NA, NIH-3T3 - in-vitro, CRC, HCT116
Cyt‑c↑, ROS↑, JNK↑,
4556- AgNPs,    Biofilm Impeding AgNPs Target Skin Carcinoma by Inducing Mitochondrial Membrane Depolarization Mediated through ROS Production
- in-vitro, Melanoma, A431
MMP↓, ROS↑, *toxicity↓, Bacteria↓,
4555- AgNPs,    Silver nanoparticles from Dendropanax morbifera Léveille inhibit cell migration, induce apoptosis, and increase generation of reactive oxygen species in A549 lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Liver, HepG2
*Bacteria↓, tumCV↓, selectivity↑, ROS↑, Apoptosis↑, TumCMig↓, AntiCan↑,
5142- AgNPs,    Biosynthesized Protein-Capped Silver Nanoparticles Induce ROS-Dependent Proapoptotic Signals and Prosurvival Autophagy in Cancer Cells
- in-vitro, CRC, HUH7
ROS↑, Apoptosis↑, eff↑, ChemoSen↑, EPR↑, Casp↑, MAPK↑,
5978- AgNPs,    Biological synthesis of silver nanoparticles and their medical applications
- Review, Var, NA
Wound Healing↑, AntiCan↑, other↑, MPT↑, ROS↑, other↑, DNAdam↑,
5977- AgNPs,  CDT,    Silver Nitroprusside as an Efficient Chemodynamic Therapeutic Agent and a Peroxynitrite nanogenerator for Targeted Cancer Therapy
- in-vivo, Ovarian, A2780S - NA, Ovarian, SKOV3
Fenton↑, ROS↑, eff↑, angioG↓, p‑Akt↓, EPR↑, selectivity↑, selectivity↑, eff↑, Cyt‑c↑, HO-1↑,
5976- AgNPs,    Review on Harnessing Silver Nanoparticles for Therapeutic Innovations: A Comprehensive Review on Medical Applications, Safety, and Future Directions
- Review, Vit, NA
*Bacteria↓, AntiCan↑, *Inflam↓, *Wound Healing↑, eff↑, ChemoSen↑, EGFR↓, ROS↑, P53↑, BAX↑, Casp3↑, toxicity↝,
5975- AgNPs,  PDT,  CDT,  RF,    Recent Advances in the Application of Silver Nanoparticles for Enhancing Phototherapy Outcomes
- Review, Var, NA - Review, BPH, NA
ROS↑, EPR↓, eff↑, Bacteria↓, eff↑, eff↑, TumVol↓,
5239- AgNPs,    NOX4- and Nrf2-mediated oxidative stress induced by silver nanoparticles in vascular endothelial cells
- in-vitro, Nor, HUVECs
*ROS↑, *Apoptosis↑, *NRF2↝,
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↓,
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↑,
5147- AgNPs,    Size dependent anti-invasiveness of silver nanoparticles in lung cancer cells
- in-vitro, Lung, A549
TumCMig↓, TumCI↓, ROS↑, p‑NF-kB↑, selectivity↑, eff↝,
5143- AgNPs,    Thermal Co-reduction engineered silver nanoparticles induce oxidative cell damage in human colon cancer cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis
- in-vitro, CRC, HCT116
ROS↑, lipid-P↑, GSH↓, MMP↓, Casp3↑, Apoptosis↑, TumCCA↑,
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↑,
4417- AgNPs,    Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways
- in-vitro, BC, MDA-MB-231
ROS↑, MDA↑, COX2↑, IL1β↑, TNF-α↑, GSH↓, Cyt‑c↑, Casp3↑, BAX↑, Bcl-2↓, LDH↓, cycD1/CCND1↓, CDK2↓, TumCCA↑, mt-Apoptosis↑,
4415- AgNPs,  SDT,  CUR,    Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells
- in-vitro, BC, MCF-7
tumCV↓, BAX↑, Casp3↑, Bcl-2↓, eff↑, ROS↑, sonoS↑, eff↑, MMP↓, Cyt‑c↑,
4414- AgNPs,    Silver nanoparticles: Forging a new frontline in lung cancer therapy
- Review, Lung, NA
tumCV↑, ROS↑, MMP↓, TumCCA↑, Apoptosis↑, angioG↓,
4413- AgNPs,  Anzaroot,    Green synthesis of silver nanoparticles from plant Astragalus fasciculifolius Bioss and evaluating cytotoxic effects on MCF7 human breast cancer cells
- in-vitro, BC, MCF-7
chemoP↑, TumCG↓, eff↑, CellMemb↑, selectivity↑, ROS↑, P53↑,
4410- AgNPs,    Green-synthesized silver nanoparticles: a sustainable nanoplatform for targeted colon cancer therapy
- Review, Colon, NA
AntiCan↑, ROS↑, mtDam↑, tumCV↓, selectivity↑,
4405- AgNPs,    Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis
- in-vitro, OS, NA
Apoptosis↑, other↑, ROS↑, eff↑, P53↝, Apoptosis↑, cl‑Casp3↑, survivin↓, MMP↓, Cyt‑c↑,
4404- AgNPs,  Rad,    Main Approaches to Enhance Radiosensitization in Cancer Cells by Nanoparticles: A Systematic Review
- Review, Var, NA
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↑,
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↑,
4439- AgNPs,    Anticancer Potential of Green Synthesized Silver Nanoparticles Using Extract of Nepeta deflersiana against Human Cervical Cancer Cells (HeLA)
- in-vitro, Cerv, HeLa
ROS↑, lipid-P↑, MMP↓, GSH↓, TumCCA↑, Apoptosis↑, Necroptosis↑, TumCD↑, Dose↝,
4549- AgNPs,    Silver nanoparticles: Synthesis, medical applications and biosafety
- Review, Var, NA - Review, Diabetic, NA
ROS↑, eff↑, other↝, DNAdam↑, EPR↑, eff↑, eff↑, TumMeta↓, angioG↓, *Bacteria↓, *eff↑, *AntiViral↑, *AntiFungal↑, eff↑, eff↑, TumCP↓, tumCV↓, P53↝, HIF-1↓, TumCCA↑, lipid-P↑, ATP↓, Cyt‑c↑, MMPs↓, PI3K↓, Akt↓, *Wound Healing↑, *Inflam↓, *Bone Healing↑, *glucose↓, *AntiDiabetic↑, *BBB↑,
4436- AgNPs,    Silver Nanoparticles (AgNPs) as Enhancers of Everolimus and Radiotherapy Sensitivity on Clear Cell Renal Cell Carcinoma
- in-vitro, Kidney, 786-O
ROS↑, MMP↑, TumCCA↑, TumCP↓, Apoptosis↑, RadioS↑,
4435- AgNPs,  Gluc,    Glucose-Functionalized Silver Nanoparticles as a Potential New Therapy Agent Targeting Hormone-Resistant Prostate Cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
selectivity↑, ROS↑, mtDam↑, TumCCA↑, TumCP↓, Apoptosis↑, MMP↓,
4433- AgNPs,    Advancements in metal and metal oxide nanoparticles for targeted cancer therapy and imaging: Mechanisms, applications, and safety concerns
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
selectivity↑, selectivity↓, mt-ROS↑,
4432- AgNPs,    Emerging nanostructure-based strategies for breast cancer therapy: innovations, challenges, and future directions
- Review, NA, NA
ROS↑, TumCP↓, Apoptosis↑,
4431- AgNPs,  doxoR,    Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1 - in-vitro, Nor, 3T3
AntiCan↑, ROS↑, TumVol↓, EPR↑, selectivity↑, ChemoSen↑,
4430- AgNPs,    Evaluation of the Genotoxic and Oxidative Damage Potential of Silver Nanoparticles in Human NCM460 and HCT116 Cells
- in-vitro, Colon, HCT116 - in-vitro, Nor, NCM460
*Bacteria↓, ROS↑, p‑p38↑, BAX↑, Bcl-2↓, BAX↑, P21↑, TumCD↑, toxicity↝,
4429- AgNPs,    Comparative proteomic analysis reveals the different hepatotoxic mechanisms of human hepatocytes exposed to silver nanoparticles
- in-vitro, Liver, HepG2
*toxicity↝, selectivity↑, mt-ROS↑,
4428- AgNPs,    p38 MAPK Activation, DNA Damage, Cell Cycle Arrest and Apoptosis As Mechanisms of Toxicity of Silver Nanoparticles in Jurkat T Cells
- in-vitro, AML, Jurkat
toxicity↝, tumCV↓, ROS↑, p38↑, NRF2↓, NF-kB↝, DNAdam↑, Apoptosis↑,
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↑,
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↓,
2286- AgNPs,    ROS_localization_after_the_silver_nanoparticles_exposure_depending_on_particle_size">Short-term changes in intracellular ROS localisation after the silver nanoparticles exposure depending on particle size
- in-vitro, Nor, 3T3
*eff↑, *mt-ROS↑, *eff↑,
2287- AgNPs,    Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine
- in-vitro, Nor, HUVECs
*TumCP↓, *ROS↑, *eff↓, *MDA↑, *GSH↓, *MMP↓, *ATP↓, *LC3II↑, *p62↑, *Bcl-2↓, *BAX↑, *Casp3↑,
2288- AgNPs,    Silver Nanoparticle-Mediated Cellular Responses in Various Cell Lines: An in Vitro Model
- Review, Var, NA
*ROS↑, Akt↓, ERK↓, DNAdam↑, Ca+2↑, ROS↑, MMP↓, Cyt‑c↑, TumCCA↑, DNAdam↑, Apoptosis↑, P53↑, p‑ERK↑, ER Stress↑, cl‑ATF6↑, GRP78/BiP↑, CHOP↑, UPR↑,
2538- AgNPs,  SDT,  Z,    Dual-functional silver nanoparticle-enhanced ZnO nanorods for improved reactive oxygen species generation and cancer treatment
- Study, Var, NA - vitro+vivo, NA, NA
ROS↑, eff↑, eff↑, TumCP↓, toxicity↓,
2835- AgNPs,  Gluc,    Carbohydrate functionalization of silver nanoparticles modulates cytotoxicity and cellular uptake
- in-vitro, Liver, HepG2
Dose↝, eff↑, ROS↑, eff↝, eff↑, eff↝, eff↑, eff↝,
2836- AgNPs,  Gluc,    Glucose capped silver nanoparticles induce cell cycle arrest in HeLa cells
- in-vitro, Cerv, HeLa
eff↝, TumCCA↑, eff↑, eff↑, ROS↑, GSH↓, SOD↓, lipid-P↑, LDH↑,
390- AgNPs,    Anti-cancerous effect of albumin coated silver nanoparticles on MDA-MB 231 human breast cancer cell line
- in-vitro, BC, MDA-MB-231 - in-vivo, BC, NA
ROS↑, TumVol↓,

Showing Research Papers: 1 to 50 of 114
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 114

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Fenton↑, 1,   GPx4↓, 1,   GSH↓, 4,   HO-1↑, 1,   lipid-P↑, 5,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 2,   ROS↑, 44,   mt-ROS↑, 2,   selenoP↓, 1,   SOD↓, 2,   TrxR↓, 2,   TrxR1↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MMP↓, 12,   MMP↑, 1,   MPT↑, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,   LDH↑, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 18,   mt-Apoptosis↑, 1,   BAX↑, 7,   Bcl-2↓, 4,   Casp↑, 2,   Casp3↑, 6,   cl‑Casp3↑, 2,   Casp9↑, 1,   Cyt‑c↑, 8,   JNK↑, 1,   MAPK↑, 1,   Necroptosis↑, 1,   p27↑, 1,   p38↑, 1,   p‑p38↑, 1,   survivin↓, 1,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

other↑, 3,   other↝, 3,   sonoS↑, 1,   tumCV↓, 7,   tumCV↑, 1,  

Protein Folding & ER Stress ⓘ

cl‑ATF6↑, 1,   CHOP↑, 1,   ER Stress↑, 4,   GRP78/BiP↑, 1,   UPR↑, 2,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 11,   P53↑, 4,   P53↝, 2,   p‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 2,   P21↑, 2,   TumCCA↑, 14,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑ERK↑, 1,   PI3K↓, 1,   TumCG↓, 2,  

Migration ⓘ

Ca+2↑, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 7,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EGFR↓, 1,   EPR↓, 1,   EPR↑, 5,   HIF-1↓, 1,   Hif1a↓, 1,   NO↑, 1,  

Barriers & Transport ⓘ

CellMemb↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↑, 1,   IL1β↑, 1,   NF-kB↝, 1,   p‑NF-kB↑, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   Dose↓, 1,   Dose↝, 3,   eff↓, 3,   eff↑, 32,   eff↝, 6,   RadioS↑, 4,   selectivity↓, 1,   selectivity↑, 17,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   LDH↓, 1,   LDH↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 8,   chemoP↑, 1,   toxicity↓, 1,   toxicity↝, 3,   TumVol↓, 3,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 106

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   MDA↑, 1,   NRF2↝, 1,   ROS↑, 5,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   JNK↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   cl‑eIF2α↑, 1,   GRP78/BiP↑, 1,   p‑PERK↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   BBB↝, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 3,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   Bone Healing↑, 1,   toxicity↓, 2,   toxicity↝, 2,   Wound Healing↑, 2,  

Infection & Microbiome ⓘ

AntiFungal↑, 1,   AntiViral↑, 2,   Bacteria↓, 4,  
Total Targets: 34

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
114 Silver-NanoParticles
4 Radiotherapy/Radiation
3 Photodynamic Therapy
3 Glucose
3 Magnetic Fields
2 Gold NanoParticles
2 chemodynamic therapy
2 SonoDynamic Therapy UltraSound
2 Curcumin
1 Copper and Cu NanoParticles
1 Chemotherapy
1 Vitamin C (Ascorbic Acid)
1 EMF
1 Anzaroot, Astragalus fasciculifolius Bioss
1 chitosan
1 doxorubicin
1 Zinc
1 Gemcitabine (Gemzar)
1 Resiquimod
1 Cisplatin
1 Camptothecin
1 entinostat
1 Alpha-Lipoic-Acid
1 Fisetin
1 Graviola
1 salinomycin
1 Selenium NanoParticles
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#:153  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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