chitosan / ROS Cancer Research Results

Chit, chitosan: Click to Expand ⟱
Features:

Chitosan — Chitosan is a deacetylated chitin-derived cationic polysaccharide used as a biocompatible biomaterial, immune-active adjuvant, and multifunctional delivery polymer rather than a standard standalone cytotoxic anticancer drug. Its formal classification is a natural polymeric biomaterial and drug-delivery excipient/platform. Standard abbreviations include CS; related derivatives include chitooligosaccharides and glycated chitosan in some oncology contexts. It is typically sourced from crustacean shells, though fungal sources also exist. In cancer research, its importance is driven mainly by mucoadhesion, protonatable amines, cargo complexation, endosomal interaction, and formulation-tunable immune and tumor-microenvironment effects; biological behavior depends strongly on molecular weight, degree of deacetylation, pattern of substitution, and formulation architecture. Low–molecular weight chitosan and modified forms have also been reported to inhibit angiogenesis, modulate tumor microenvironment acidity, interfere with metastasis, and induce apoptosis in some in vitro systems. A major translational role of chitosan is as a nanoparticle carrier for chemotherapeutics, genes, and immunotherapies, improving stability and targeted delivery. Effects vary significantly depending on molecular weight, degree of deacetylation, and formulation.

Primary mechanisms (ranked):

Chitosan has been shown to inhibit the growth of various types of cancer cells, including breast, lung, and colon cancer cells.
Chitosan has been shown to inhibit angiogenesis, stimulate the immune system, and anti-inflammatory.

Chitosan is only soluble in acidic settings, hence limiting its use in neutral or alkaline pH circumstances
  1. Drug and gene delivery enhancement via cationic complexation, mucoadhesion, cellular uptake facilitation, and controlled/stimuli-responsive release
  2. Innate immune activation and adjuvanticity, including dendritic-cell and macrophage engagement with downstream NK-cell support
  3. Tumor microenvironment and cytokine modulation, which can favor antitumor immune tone in selected formulations
  4. Direct antiproliferative and pro-apoptotic signaling in cancer cells, usually derivative-, molecular-weight-, and formulation-dependent rather than a robust native-CS class effect
  5. Anti-migratory and anti-invasive effects, including reported suppression of MMP-linked metastatic behavior in some models
  6. Anti-angiogenic effects in selected low-molecular-weight or modified systems
  7. Secondary redox modulation, usually downstream of formulation or cell-stress effects rather than a core redox pharmacology

Bioavailability / PK relevance: Chitosan is not a conventional systemically bioavailable small molecule. Native CS has limited neutral-pH solubility and its translational behavior is dominated by route, particle size, surface chemistry, molecular weight, and degree of deacetylation. Oncology relevance is strongest in local, mucosal, intratumoral, hydrogel, nanoparticle, and carrier-based applications rather than free systemic exposure.

In-vitro vs systemic exposure relevance: Many direct in-vitro anticancer studies use concentrations, contact conditions, or modified chitosan constructs that are not straightforwardly comparable to achievable systemic exposure of native CS. Therefore, carrier/platform effects and local-delivery applications are more clinically plausible than relying on native chitosan as a systemic concentration-driven anticancer agent.

Clinical evidence status: Predominantly preclinical for direct anticancer use. Human oncology evidence is limited and mostly adjunctive, formulation-specific, or device/supportive-care related. There is no established regulatory status for chitosan as a standalone approved anticancer drug, although chitosan-containing or chitosan-derived oncology platforms and local immunotherapy approaches have entered early clinical investigation.

Mechanistic pathway table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Drug and gene delivery platform Drug uptake ↑; nucleic-acid delivery ↑; tumor retention ↑ (formulation-dependent) Off-target exposure ↓ (potential); mucosal penetration ↑ P, R, G Therapeutic leverage platform Most clinically relevant oncology role. Cationic amino groups enable cargo binding, surface functionalization, and controlled release; many benefits are formulation-driven rather than intrinsic cytotoxicity.
2 Innate immune activation and adjuvanticity Immune-mediated tumor pressure ↑; DC activation ↑; NK support ↑ Innate immune responsiveness ↑ R, G Immunostimulatory Chitosan and some derivatives act as immune adjuvants and can enhance antigen presentation and antitumor immune priming.
3 Cytokine and tumor microenvironment modulation Pro-tumor immune suppression ↓ (context-dependent); IL-12 / IFN-γ / TNF-α tone ↑ (reported) Immune tone ↔ or ↑ R, G Microenvironment remodeling Relevant mainly in immune-active formulations such as nanoparticles, vaccine adjuvants, and glycated chitosan-based local immunotherapy systems.
4 Apoptosis and mitochondrial stress Apoptosis ↑; MMP ↓; caspase signaling ↑ (derivative-dependent) Usually milder injury at comparable exposures G Context-dependent direct anticancer effect Direct tumor-cell killing is reported, but is much less uniform than delivery/immunology effects and depends strongly on molecular weight, substitution, and nanoformulation.
5 Migration invasion and metastasis axis MMP2 ↓; MMP9 ↓; migration ↓; invasion ↓ ↔ G Anti-metastatic Often observed in modified chitosans or drug-loaded systems; likely linked to altered adhesion, matrix interaction, and signaling restraint.
6 Angiogenesis signaling VEGF axis ↓ (context-dependent); neovascular support ↓ ↔ G Anti-angiogenic Reported mainly for low-molecular-weight or chemically modified chitosan systems and for payload-enabled constructs.
7 Mitochondrial ROS increase (secondary) ROS ↑ or ↔ (model-dependent); oxidative stress ↑ (high concentration only) ROS ↓ or ↔ in some protective contexts R, G Secondary stress modulation Redox behavior is inconsistent across systems and should not be treated as a primary class-defining mechanism for native chitosan.
8 Clinical Translation Constraint Standalone systemic anticancer efficacy uncertain; heterogeneity ↑ Biocompatibility generally favorable, but local irritation / allergy concerns remain — Translation constraint Key limitations are poor neutral-pH solubility of native CS, batch heterogeneity, scale-up and characterization issues, route dependence, and the gap between promising preclinical carrier systems and sparse oncology trial validation.
TSF: P = 0–30 min (surface interactions), R = 30 min–3 hr (immune signaling shifts), G = >3 hr (phenotype and immune outcomes).



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⟱
4399- AgNPs,  Chit,    Silver nanoparticles impregnated alginate-chitosan-blended nanocarrier induces apoptosis in human glioblastoma cells
- in-vitro, GBM, U87MG
DNAdam↑, ROS↑, MMP↓, eff↑,
1405- BBR,  Chit,    Chitosan/alginate nanogel potentiate berberine uptake and enhance oxidative stress mediated apoptotic cell death in HepG2 cells
- in-vitro, Liver, HepG2
*BioAv↑, ROS↑, MMP↓, TumCP↓,
6001- Chit,    Recent advances in engineering chitosan-based nanoplatforms in biotherapeutic multi-delivery for multi-targeted disease treatments: Promises and outlooks
- Review, Var, HepG2 - Review, AD, NA
TumVol↓, toxicity↓, Half-Life↑, eff↑, selectivity↑, Dose↝, *BDNF↑, *NRF2↑, *ROS↓, *neuroP↑, *memory↑, *cognitive↑, *Obesity↓,
5988- Chit,    Chitosan immunomodulation: insights into mechanisms of action on immune cells and signaling pathways
- Review, Var, NA
DDS↑, *Cartilage↑, *Wound Healing↑, Imm↑, cGAS–STING↑, STAT1↑, NLRP3↑, *DCells↑, *IL10↓, *TGF-β1↓, *TNF-α↓, IL1β↓, ROS↑,
5990- Chit,    Chitosan Nanoparticles for Targeted Cancer Therapy: A Review of Stimuli-Responsive, Passive, and Active Targeting Strategies
- Review, Var, NA
DDS↑, eff↓, *Bacteria↓, *antiOx↑, *Wound Healing↑, *Imm↑, TumCP↓, TumMeta↓, angioG↓, Apoptosis↑, ROS↑, ER Stress↑, BioAv↑, Half-Life↑, eff↑, EPR↑, ChemoSen↑, eff↑,
5991- Chit,    Chitosan-Based Nanoencapsulated Essential Oils: Potential Leads against Breast Cancer Cells in Preclinical Studies
- Review, BC, NA
*other↝, *BioAv↓, eff↑, toxicity↓, eff↑, TumCD↑, Half-Life↑, selectivity↑, EPR↑, ROS↑, Apoptosis↑, eff↑,
5994- Chit,    Anticancer Activity of Chitosan, Chitosan Derivatives, and Their Mechanism of Action
- Review, Var, NA
angioG↓, *Imm↑, *antiOx↑, selectivity↑, other↝, toxicity↓, BioAv↑, eff↝, Half-Life↑, MPT↑, MMP9↓, lipid-P↑, EPR↑, NK cell↑, Casp3↑, Casp8↑, TumCCA↑, ROS↑, DDS↑, VEGF↓, TIMP1↑, ChemoSen↑, eff↑,
5995- Chit,  CUR,    Enhancement of anticancer activity and drug delivery of chitosan-curcumin nanoparticle via molecular docking and simulation analysis
- vitro+vivo, Var, NA
eff↑, EPR↑, DNAdam↑, TumCCA↑, ROS↑, toxicity↓,
4478- Chit,    Chitosan promotes ROS-mediated apoptosis and S phase cell cycle arrest in triple-negative breast cancer cells: evidence for intercalative interaction with genomic DNA
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, BC, T47D
TumCP↓, selectivity↑, MMP↓, ROS↑, TumCCA↑, Apoptosis↑, Casp3↑,
4479- Chit,    Chitosan nanoparticles triggered the induction of ROS-mediated cytoprotective autophagy in cancer cells
- in-vitro, Cerv, HeLa - in-vitro, HCC, SMMC-7721 cell
TumAuto↑, ROS↑, eff↓,
4481- Chit,    Antioxidant Properties and Redox-Modulating Activity of Chitosan and Its Derivatives: Biomaterials with Application in Cancer Therapy
- Review, Var, NA
*BioAv↑, *toxicity↓, *antiOx↑, AntiCan↑, *Inflam↓, *ROS↓, *lipid-P↓, MDA↓, selectivity↑, MMP↓, ROS↑, TumCCA↑, MDA↑, GSH↓, ChemoSen↑,
4482- Chit,    Hyaluronic acid-coated chitosan nanoparticles induce ROS-mediated tumor cell apoptosis and enhance antitumor efficiency by targeted drug delivery via CD44
- in-vitro, Lung, A549 - in-vitro, Liver, HepG2
EPR↑, mtDam↑, ROS↑, Apoptosis↑,
2968- PL,  Chit,    Preparation of piperlongumine-loaded chitosan nanoparticles for safe and efficient cancer therapy
- in-vitro, GC, AGS
eff↑, Dose↝, ROS↑, BioAv↑,
6051- RES,  SeNPs,  Chit,    Resveratrol-loaded selenium/chitosan nano-flowers alleviate glucolipid metabolism disorder-associated cognitive impairment in Alzheimer's disease
- in-vivo, AD, NA
*Inflam↓, *ROS↓, *GutMicro↑, *lipid-P↓, *Aβ↓, *tau↓, *cognitive↑,
4483- Se,  Chit,    Anti-cancer potential of chitosan-starch selenium Nanocomposite: Targeting osteoblastoma and insights of molecular docking
- in-vitro, OS, NA
AntiCan↑, TumCP↓, Apoptosis↑, ROS↑, eff↑, other↝, eff↑, TumCCA↑,
4484- Se,  Chit,  PEG,    Anti-cancer potential of selenium-chitosan-polyethylene glycol-carvacrol nanocomposites in multiple myeloma U266 cells
- in-vitro, Melanoma, U266
tumCV↓, selectivity↑, ROS↑, MMP↓, Apoptosis↑, BAX↑, Casp3↑, Casp9↑, Bcl-2↓,
4486- Se,  Chit,    Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis
- in-vitro, Liver, HepG2
Apoptosis↑, TumCCA↑, MMP↓, Bcl-2↓, BAX↑, cl‑Casp9↑, cl‑Casp3↑, Risk↓, *BioAv↑, *toxicity↑, TumCG↓, AntiTum↑, ROS↑, Cyt‑c↑, Fas↑, FasL↑, FADD↑,
4480- SeNPs,  Chit,    Biogenic synthesized selenium nanoparticles combined chitosan nanoparticles controlled lung cancer growth via ROS generation and mitochondrial damage pathway
- in-vitro, Lung, A549 - in-vitro, Nor, HK-2
selectivity↑, *toxicity↓, ROS↑, mtDam↑, Apoptosis↑, LDH↑,
4452- SeNPs,  Chit,    Antioxidant capacities of the selenium nanoparticles stabilized by chitosan
- in-vitro, Nor, 3T3
*toxicity↓, *antiOx↑, *GPx↑, *ROS↓,
4491- SeNPs,  Chit,  VitC,    Synthesis of a Bioactive Composition of Chitosan–Selenium Nanoparticles
- Study, NA, NA
*ROS↓, *selenoP↑, *antiOx↑, *Inflam↓, *Risk↓, *toxicity↓, AntiTum↑, Dose↝,

Showing Research Papers: 1 to 20 of 20

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 20

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   lipid-P↑, 1,   MDA↓, 1,   MDA↑, 1,   ROS↑, 16,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 6,   MPT↑, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

LDH↑, 1,  

Cell Death ⓘ

Apoptosis↑, 8,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   FADD↑, 1,   Fas↑, 1,   FasL↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 2,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

STAT1↑, 1,   TumCG↓, 1,  

Migration ⓘ

MMP9↓, 1,   TIMP1↑, 1,   TumCP↓, 4,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EPR↑, 5,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Imm↑, 1,   NK cell↑, 1,  

Cellular Microenvironment ⓘ

cGAS–STING↑, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,   ChemoSen↑, 3,   DDS↑, 3,   Dose↝, 3,   eff↓, 2,   eff↑, 12,   eff↝, 1,   Half-Life↑, 4,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

LDH↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 2,   Risk↓, 1,   toxicity↓, 4,   TumVol↓, 1,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 5,   GPx↑, 1,   lipid-P↓, 2,   NRF2↑, 1,   ROS↓, 5,   selenoP↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Migration ⓘ

Cartilage↑, 1,   TGF-β1↓, 1,  

Immune & Inflammatory Signaling ⓘ

DCells↑, 1,   IL10↓, 1,   Imm↑, 2,   Inflam↓, 3,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 3,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 2,   memory↑, 1,   neuroP↑, 1,   Obesity↓, 1,   Risk↓, 1,   toxicity↓, 4,   toxicity↑, 1,   Wound Healing↑, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 29

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
20 chitosan
4 Selenium NanoParticles
3 Selenium
1 Silver-NanoParticles
1 Berberine
1 Curcumin
1 Piperlongumine
1 Resveratrol
1 polyethylene glycol
1 Vitamin C (Ascorbic Acid)
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#:210  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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