Silver-NanoParticles / Casp3 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)


Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
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↑,
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↝,
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↓,
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↑,
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↑,
4438- AgNPs,  ART/DHA,    Biogenic synthesis of AgNPs using Artemisia oliveriana extract and their biological activities for an effective treatment of lung cancer
- in-vitro, Lung, A549
EPR↑, BAX↑, Bcl-2↑, Casp3↑, Casp9↑, DNAdam↑, TumCCA↑, Apoptosis↑,
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↑,
398- AgNPs,    Silver nanoparticles induced testicular damage targeting NQO1 and APE1 dysregulation, apoptosis via Bax/Bcl-2 pathway, fibrosis via TGF-β/α-SMA upregulation in rats
- in-vivo, Testi, NA
Bcl-2↓, Casp3↑, GSH↓, MDA↑, NO↑, H2O2↑, SOD↓,
393- AgNPs,    Green synthesized plant-based silver nanoparticles: therapeutic prospective for anticancer and antiviral activity
- in-vitro, NA, HCT116
mtDam↑, ROS↑, TumCCA↑, Casp3↑, BAX↑, Bcl-2↓, P53↑,
397- AgNPs,  GEM,    Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment
- in-vitro, Ovarian, A2780S
P53↑, P21↑, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, Bcl-2↓, ROS↑, MMP↓,
400- AgNPs,  MF,    Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field
- in-vitro, Laryn, HEp2
TumCP↓, Casp3↑, P53↑, Beclin-1↑, TumAuto↑, GSR↑, ROS↑, MDA↑, ROS↑, SIRT1↑, Ca+2↑, Endon↑, DNAdam↑, Apoptosis↑, NF-kB↓,
4388- AgNPs,    Differential Cytotoxic Potential of Silver Nanoparticles in Human Ovarian Cancer Cells and Ovarian Cancer Stem Cells
- in-vitro, Cerv, NA
tumCV↓, CSCs↓, selectivity↑, Apoptosis↑, ROS↑, LDH↓, Casp3↑, BAX↑, Bak↑, cMyc↑, MMP↓,
334- AgNPs,    Silver-Based Nanoparticles Induce Apoptosis in Human Colon Cancer Cells Mediated Through P53
- in-vitro, Colon, HCT116
Bax:Bcl2↑, P53↑, P21↑, Casp3↑, Casp8↑, Casp9↑, Akt↓, NF-kB↓, DNAdam↑, TumCCA↑,
346- AgNPs,  RSQ,    Investigating Silver Nanoparticles and Resiquimod as a Local Melanoma Treatment
- in-vivo, Melanoma, SK-MEL-28 - in-vivo, Melanoma, WM35
ROS↑, Ca+2↝, Casp3↑, Casp8↑, Casp9↑, CD4+↑, CD8+↑, tumCV↓, eff↓, *toxicity↓,
348- AgNPs,    Induction of p53 mediated mitochondrial apoptosis and cell cycle arrest in human breast cancer cells by plant mediated synthesis of silver nanoparticles from Bergenia ligulata (Whole plant)
- in-vitro, BC, MCF-7
Apoptosis↑, ROS↑, MMP↓, P53↑, BAX↑, cl‑Casp3↑,
350- AgNPs,    Cytotoxic and Apoptotic Effects of Green Synthesized Silver Nanoparticles via Reactive Oxygen Species-Mediated Mitochondrial Pathway in Human Breast Cancer Cells
- in-vitro, BC, MCF-7
ROS↑, MMP↓, P53↑, BAX↑, Casp3↑, Casp9↑, Bcl-2↓,
351- AgNPs,    Study of antitumor activity in breast cell lines using silver nanoparticles produced by yeast
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D
Casp9↑, Casp3↑, Casp7↑, Bcl-2↓,
388- AgNPs,    Apoptotic efficacy of multifaceted biosynthesized silver nanoparticles on human adenocarcinoma cells
- in-vitro, BC, MCF-7
ROS↑, Casp3↑, BAX↑, P53↑, Casp↑, Cyt‑c↑, MMP↓, DNAdam↑, Bcl-2↓, BAX↑,
324- AgNPs,  CPT,    Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells
- in-vitro, Cerv, HeLa
ROS↑, Casp3↑, Casp9↑, Casp6↑, GSH↓, SOD↓, GPx↓, MMP↓, P53↑, P21↑, Cyt‑c↑, BID↑, BAX↑, Bcl-2↓, Bcl-xL↓, Akt↓, Raf↓, ERK↓, MAP2K1/MEK1↓, JNK↑, p38↑,
327- AgNPs,  MS-275,    Combination Effect of Silver Nanoparticles and Histone Deacetylases Inhibitor in Human Alveolar Basal Epithelial Cells
- in-vitro, Lung, A549
Apoptosis↑, ROS↑, LDH↓, TNF-α↑, mtDam↑, TumAuto↑, Casp3↑, Casp9↑, DNAdam↑,
379- AgNPs,    Effects of green-synthesized silver nanoparticles on lung cancer cells in vitro and grown as xenograft tumors in vivo
- in-vivo, Lung, H1299
NF-kB↓, Bcl-2↓, Casp3↑, survivin↑, TumCG↓,
377- AgNPs,    Anticancer Action of Silver Nanoparticles in SKBR3 Breast Cancer Cells through Promotion of Oxidative Stress and Apoptosis
- in-vitro, BC, SkBr3
ROS↑, Apoptosis↑, Bax:Bcl2↑, VEGF↑, Akt↓, PI3K↓, TAC↓, TOS↑, OSI↑, MDA↑, Casp3↑, Casp7↑,
381- AgNPs,    Silver Nanoparticles Exert Apoptotic Activity in Bladder Cancer 5637 Cells Through Alteration of Bax/Bcl-2 Genes Expression
- in-vitro, Bladder, 5637
ROS↑, BAX↑, Bcl-2↓, Casp3↑, Casp7↑, Apoptosis↑,
384- AgNPs,    Dual functions of silver nanoparticles in F9 teratocarcinoma stem cells, a suitable model for evaluating cytotoxicity- and differentiation-mediated cancer therapy
- in-vitro, Testi, F9
LDH↓, ROS↑, mtDam↑, DNAdam↑, P53↑, P21↑, BAX↑, Casp3↑, Bcl-2↓, Casp9↑, Nanog↓, OCT4↓,
386- AgNPs,  Tam,    Synergistic anticancer effects and reduced genotoxicity of silver nanoparticles and tamoxifen in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
P53↑, BAX↑, Bcl-2↓, Casp3↑, DNAdam↑, TumCCA↑,
387- AgNPs,    Silver nanoparticles induce mitochondria-dependent apoptosis and late non-canonical autophagy in HT-29 colon cancer cells
- in-vitro, Colon, HT-29
Cyt‑c↑, P53↑, BAX↑, Casp3↑, Casp9↑, Casp12↑, Beclin-1↑, CHOP↑, LC3s↑, XBP-1↑,
369- AgNPs,    Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis
- in-vitro, Liver, NA
ROS↑, GSH↓, DNAdam↑, lipid-P↝, Apoptosis↑, BAX↑, Bcl-2↓, MMP↓, Casp9↑, Casp3↑, JNK↑,
359- AgNPs,    Anti-cancer & anti-metastasis properties of bioorganic-capped silver nanoparticles fabricated from Juniperus chinensis extract against lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Nor, HEK293
Casp3↑, Casp9↑, P53↑, ROS↑, MMP2↓, MMP9↓, TumCCA↑, *toxicity↓, TumCMig↓, TumCI↓,
358- AgNPs,    Preparation of triangular silver nanoparticles and their biological effects in the treatment of ovarian cancer
- vitro+vivo, Ovarian, SKOV3
TumCCA↑, ROS↑, Casp3↑, TumCG↓, cycD1/CCND1↓,
363- AgNPs,    Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis
ROS↑, lipid-P↑, Apoptosis↑, BAX↑, Bcl-2↓, MMP↓, Cyt‑c↑, Casp3↑, Casp9↑, JNK↑,
848- Gra,  AgNPs,    Synthesis, Characterization and Evaluation of Antioxidant and Cytotoxic Potential of Annona muricata Root Extract-derived Biogenic Silver Nanoparticles
- in-vitro, CRC, HCT116
ROS↑, PUMA↝, Casp3↑, Casp8↑, Casp9↑, Apoptosis↑,
323- Sal,  AgNPs,    Combination of salinomycin and silver nanoparticles enhances apoptosis and autophagy in human ovarian cancer cells: an effective anticancer therapy
- in-vitro, BC, MDA-MB-231 - in-vitro, Ovarian, A2780S
TumCD↑, LDH↓, MDA↑, SOD↓, ROS↑, GSH↓, Catalase↓, MMP↓, P53↑, P21↑, BAX↑, Bcl-2↓, Casp3↑, Casp9↑, Apoptosis↑, TumAuto↑,

Showing Research Papers: 1 to 35 of 35

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 35

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx↓, 1,   GSH↓, 6,   GSR↑, 1,   H2O2↑, 1,   lipid-P↑, 2,   lipid-P↝, 1,   MDA↑, 5,   NRF2↑, 1,   OSI↑, 1,   ROS↑, 28,   SOD↓, 3,   TAC↓, 1,   TOS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 13,   mtDam↑, 3,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↑, 1,   LDH↓, 5,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 15,   mt-Apoptosis↑, 1,   Bak↑, 2,   BAX↑, 21,   Bax:Bcl2↑, 2,   Bcl-2↓, 17,   Bcl-2↑, 1,   Bcl-xL↓, 1,   BID↑, 1,   Casp↑, 1,   Casp12↑, 1,   Casp3↑, 31,   cl‑Casp3↑, 3,   Casp6↑, 1,   Casp7↑, 3,   Casp8↑, 3,   Casp9↑, 16,   Cyt‑c↑, 9,   Endon↑, 1,   JNK↑, 3,   p27↑, 1,   p38↑, 1,   PUMA↝, 1,   survivin↓, 1,   survivin↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

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

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 2,   LC3s↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 8,   P53↑, 15,   P53↝, 1,   p‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 3,   P21↑, 6,   TumCCA↑, 9,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   ERK↓, 1,   MAP2K1/MEK1↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   TumCG↓, 2,  

Migration ⓘ

Ca+2↑, 1,   Ca+2↝, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   EPR↑, 1,   NO↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↑, 1,   IL1β↑, 1,   NF-kB↓, 3,   TNF-α↑, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↓, 1,   eff↑, 5,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   LDH↓, 5,  

Functional Outcomes ⓘ

AntiCan↑, 2,   toxicity↝, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 95

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   MDA↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 16

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
35 Silver-NanoParticles
1 SonoDynamic Therapy UltraSound
1 Curcumin
1 Artemisinin
1 Gemcitabine (Gemzar)
1 Magnetic Fields
1 Resiquimod
1 Camptothecin
1 entinostat
1 tamoxifen
1 Graviola
1 salinomycin
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#:42  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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