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


Nor, Normal Healthy: Click to Expand ⟱
Normal Healthy
Scientific Papers found: Click to Expand⟱
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↑,
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↓,
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↑,
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↑,
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↑,
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↝,
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↑,
4369- AgNPs,    Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells
- in-vitro, Nor, BEAS-2B
*ROS↑,
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↑,
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↓,
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↑,
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↑,
2000- AL,    Exploring the ROS-mediated anti-cancer potential in human triple-negative breast cancer by garlic bulb extract: A source of therapeutically active compounds
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, NA
selectivity↑, TumCG?, *toxicity∅, ROS↑, MMP↓, TumCCA↑, P53↑, Bcl-2↓, p‑Akt↓, p‑p38↓, *ROS∅,
1069- AL,    Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling
- vitro+vivo, ESCC, TE1 - vitro+vivo, ESCC, KYSE-510 - in-vitro, Nor, Het-1A
TumCP↓, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, p‑AMPK↑, mTOR↓, TumAuto↑, NCOA4↑, MDA↑, Iron↑, TumW↓, TumVol↓, ATG5↑, ATG7↑, TfR1/CD71↓, FTH1↓, ROS↑, Iron↑, Ferroptosis↑, *toxicity↓,
5167- AL,    The Effects of Allicin, a Reactive Sulfur Species from Garlic, on a Selection of Mammalian Cell Lines
- in-vitro, Nor, 3T3 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, CRC, HT-29
Thiols↓, tumCV↓, TumCP↓, GSH↓, GSSG↑, ROS↑,
3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, TumCMig↓, TumCI↓, ROS↑, Hif1a↑, JNK↑, Casp↑, TumCCA↑, Apoptosis↑, selectivity↑,
1235- ALA,  Cisplatin,    α-Lipoic acid prevents against cisplatin cytotoxicity via activation of the NRF2/HO-1 antioxidant pathway
- in-vitro, Nor, HEI-OC1 - ex-vivo, NA, NA
ROS↑, HO-1↓, *toxicity↓, chemoP↑, *ROS↓, *HO-1↑, *SOD1↑, *NRF2↑,
1999- Api,  doxoR,    Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation
- in-vitro, Nor, NRK52E - in-vitro, Nor, MPC5 - in-vitro, BC, 4T1 - in-vivo, NA, NA
neuroP↑, ChemoSen∅, RenoP↑, selectivity↑, chemoP↑, ROS↑, *ROS∅, *antiOx↑, *toxicity↓,
1565- Api,    Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H1975
TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, Cyt‑c↑, MDA↑, GSH↓, ROS↑, PI3K↓, Akt↓, mTOR↓,
1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, selectivity↑, selectivity↓, ROS↑, eff↑, tumCV↓, MMP↓, Dose∅, eff↓, DNAdam↑, Apoptosis↑, TumAuto↑, Necroptosis↑, p‑P53↑, BIM↑, BAX↑, p‑PARP↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Bcl-2↓, AIF↑, p62↑, LC3B↑, MLKL↑, p‑MLKL↓, RIP3↑, p‑RIP3↑, TumCG↑, TumW↓,
2570- ART/DHA,    Discovery, mechanisms of action and combination therapy of artemisinin
- Review, Nor, NA
*BioAv↓, *Half-Life↓, *toxicity↓, *ROS↑, GSH↓, selectivity↑,
1142- Ash,    Ashwagandha-Induced Programmed Cell Death in the Treatment of Breast Cancer
- Review, BC, MCF-7 - NA, BC, MDA-MB-231 - NA, Nor, HMEC
Apoptosis↑, ROS↑, DNAdam↑, OXPHOS↓, *ROS∅, Bcl-2↓, XIAP↓, survivin↓, DR5↑, IKKα↓, NF-kB↓, selectivity↑, *ROS∅, eff↓, Paraptosis↑,
3172- Ash,    Implications of Withaferin A for the metastatic potential and drug resistance in hepatocellular carcinoma cells via Nrf2-mediated EMT and ferroptosis
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
Keap1↑, NRF2↓, EMT↓, TumCP↓, TumCI↓, selectivity↑, *toxicity↓, ROS↑, MDA↑, GSH↓, Ferroptosis↑,
1355- Ash,    Withaferin A-Induced Apoptosis in Human Breast Cancer Cells Is Mediated by Reactive Oxygen Species
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, HMEC
eff↑, mt-ROS↑, mitResp↓, OXPHOS↓, compIII↑, BAX↑, Bak↑, other↓, ATP∅, *ROS∅,
2003- Ash,    Withaferin A Induces Cell Death Selectively in Androgen-Independent Prostate Cancer Cells but Not in Normal Fibroblast Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Nor, TIG-1 - in-vitro, PC, LNCaP
TumCD↑, selectivity↑, cFos↑, ROS↑, *ROS∅, HSP70/HSPA5↑, Apoptosis↑, ER Stress↑, TumCCA↑,
1533- Ba,    Baicalein, as a Prooxidant, Triggers Mitochondrial Apoptosis in MCF-7 Human Breast Cancer Cells Through Mobilization of Intracellular Copper and Reactive Oxygen Species Generation
- in-vitro, BrCC, MCF-7 - in-vitro, Nor, MCF10
tumCV↓, i-ROS↑, MMP↓, Bcl-2↓, BAX↑, Cyt‑c↑, Casp9↑, Casp3↑, eff↓, selectivity↑, *toxicity∅, Apoptosis↑, Fenton↑,
1523- Ba,    ROS-induced_BNIP3_expression">Baicalein induces human osteosarcoma cell line MG-63 apoptosis via ROS-induced BNIP3 expression
- in-vitro, OS, MG63 - in-vitro, Nor, hFOB1.19
TumCD↑, Apoptosis↑, ROS↑, eff↓, Casp3↑, Bcl-2↓, selectivity↑, Cyt‑c↑, LDH?, BNIP3?, BAX↑,
2474- Ba,    Anticancer properties of baicalein: a review
- Review, Var, NA - in-vitro, Nor, BV2
ROS⇅, ROS↑, ER Stress↑, Ca+2↑, Apoptosis↑, eff↑, DR5↑, 12LOX↓, Cyt‑c↑, Casp7↑, Casp9↑, Casp3↑, cl‑PARP↑, TumCCA↑, cycE/CCNE↑, CDK4↓, cycD1/CCND1↓, VEGF↓, cMyc↓, Hif1a↓, NF-kB↓, BioEnh↑, BioEnh↑, P450↓, *Hif1a↓, *iNOS↓, *COX2↓, *VEGF↓, *ROS↓, *PI3K↓, *Akt↓,
2023- BBR,    Berberine Induces Caspase-Independent Cell Death in Colon Tumor Cells through Activation of Apoptosis-Inducing Factor
- in-vitro, Colon, NA - in-vitro, Nor, YAMC
TumCD↑, *toxicity↓, selectivity↑, ROS↑, *ROS∅, MMP↓, *MMP∅, PARP↑, BioAv↝,
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, IL6↓, MCP1↓, COX2↓, PGE2↓, MMP2↓, MMP9↓, DNAdam↑, eff↝, Telomerase↓, Bcl-2↓, AMPK↑, ROS↑, MMP↓, ATP↓, p‑mTORC1↓, p‑S6K↓, ERK↓, PI3K↓, PTEN↑, Akt↓, Raf↓, MEK↓, Dose↓, Dose↑, selectivity↑, TumCCA↑, eff↑, EGFR↓, Glycolysis↓, Dose?, p27↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycE/CCNE↓, Bax:Bcl2↑, Casp3↑, Casp9↑, VEGFR2↓, ChemoSen↑, eff↑, eff↑, PGE2↓, JAK2↓, STAT3↓, CXCR4↓, CCR7↓, uPA↓, CSCs↓, EMT↓, Diff↓, CD133↓, Nestin↓, n-MYC↓, NOTCH↓, SOX2↓, Hif1a↓, VEGF↓, RadioS↑,
2739- BetA,    Glycolytic Switch in Response to Betulinic Acid in Non-Cancer Cells
- in-vitro, Nor, HUVECs - in-vitro, Nor, MEF
*Glycolysis↑, *GlucoseCon↑, *Apoptosis↓, *UCP1↓, *AMPK↑, GLUT1↑, mt-ROS↑,
1566- betaCar,  Lyco,    Antioxidant and pro-oxidant effects of lycopene in comparison with beta-carotene on oxidant-induced damage in Hs68 cells
- in-vitro, Nor, HS68
*ROS↑, *ROS⇅, *Dose?,
1421- Bos,    Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes
- in-vitro, AML, HL-60 - in-vitro, Nor, NA
ROS↑, NADPH↝, 5LO↓, Ca+2↑, p38↑, p42↑,
2024- Bos,    Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
MMP↓, Cyt‑c↑, ROS↑, Casp8↑, Casp9↑, AntiTum↑, selectivity↑, TumCCA↑,
1447- Bos,    Boswellia carterii n-hexane extract suppresses breast cancer growth via induction of ferroptosis by downregulated GPX4 and upregulated transferrin
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vivo, BC, 4T1 - in-vitro, Nor, MCF10
tumCV↓, AntiCan↑, *toxicity↓, Ferroptosis↑, i-Iron↑, GPx4↓, ROS↑, lipid-P↑, Tf↑, TumCG↓,
2047- Buty,    Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells
- in-vitro, CRC, T24/HTB-9 - in-vitro, Nor, SV-HUC-1 - in-vitro, Bladder, 5637 - in-vivo, NA, NA
HDAC↓, AntiTum↑, TumCMig↓, AMPK↑, mTOR↑, TumAuto↑, ROS↑, miR-139-5p↑, BMI1↓, TumCI?, E-cadherin↑, N-cadherin↓, Vim↓, Snail↓, cl‑PARP↑, cl‑Casp3↑, BAX↑, Bcl-2↓, Bcl-xL↓, MMP↓, PINK1↑, PARK2↑, TumMeta↓, TumCG↓, LC3II↑, p62↓, eff↓,
5842- CAP,    Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses
- Review, Nor, NA - Review, Diabetic, NA
*Pain↓, *TRPV1↑, AMPK↑, ROS↑, TumCP↑, Apoptosis↑, TumCCA↑, Casp3↑, BAX↑, Bak↑, cl‑PARP↑, Bcl-2↓, RNS↑, *glucose↓, *Insulin↑, *BP↓, *AntiAg↑, ER Stress↑, Hif1a↓, chemoPv↑,
5858- CAP,    Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health
- Review, Nor, NA - Review, AD, NA
*BBB↓, *GutMicro↑, Obesity↓, *Inflam↓, *AntiCan↑, *TRPV1↑, *Ca+2↑, *antiOx↑, *cardioP↑, *BioAv↓, *Half-Life↓, *BioAv↝, *BioAv↑, *neuroP↑, Apoptosis↑, p38↑, ROS↑, MMP↓, MPT↑, Cyt‑c↑, Casp↑, TRIB3↑, NADH↓, SIRT1↓, TumCG↓, TumCMig↓, TOP1↓, TOP2↓, β-catenin/ZEB1↓, *ROS↓, *Aβ↓,
2014- CAP,    Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, Bxpc-3 - in-vitro, Nor, HPDE-6 - in-vivo, PC, AsPC-1
ROS↑, *ROS∅, selectivity↑, compI↓, compIII↓, eff↑, selectivity↑, ATP↓, Cyt‑c↑, Casp9↑, Casp3↑, MMP↓, SOD↓, GSH/GSSG↓, Apoptosis↑, *toxicity∅, GSH↓, Catalase↓, GPx↓, Dose↝,
5881- CAR,    Carvacrol—A Natural Phenolic Compound with Antimicrobial Properties
- Review, Nor, NA
*Bacteria↓, *Inflam↓, *SOD↑, *GPx↑, *GSR↑, *Catalase↑, *toxicity↓, *Pain↓, *other↑, *cardioP↑, *RenoP↑, *neuroP↑, *antiOx↑, *AntiDiabetic↑, *hepatoP↑, *Obesity↓, *AntiAg↑, *BioAv↓, BioAv↝, *OS↑, MMP↓, ROS↑, *MDA↓, *lipid-P↓, *COX2↓, *Dose↝,
5880- CAR,    In vitro and in vivo antitumor potential of carvacrol nanoemulsion against human lung adenocarcinoma A549 cells via mitochondrial mediated apoptosis
- vitro+vivo, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, PC9
Dose↝, mt-ROS↑, p‑JNK↑, BAX↑, Cyt‑c↑, Casp↑, AntiTum↑, ER Stress↑, LDH↑, selectivity↑, Apoptosis↑, DNAdam↑, IRE1↑, XBP-1↑, CHOP↓, p‑eIF2α↓, GRP78/BiP↓, Ca+2↑, MMP↓, Bcl-2↓, Casp3↑, Casp9↑, eff↓, TumW↓, Weight↑, eff↑, eff↑,
6027- CGA,  CUR,  EGCG,  QC,  RES  Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol
- Review, Nor, NA
*ROS↓, ROS↑,
6108- Chol,    Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health
- Review, Nor, NA - Review, AD, NA
*TMAO↑, *ROS↑, *NADPH↑, *Ca+2↑, *AntiAg↓, *cognitive↓, *TJ↓, *CLDN1↓, *ZO-1↓, *Inflam↑, *NLRP3↑, *ER Stress↑, *cognitive↓, *Dose↝, *eff↑, *other↝, *other↝, *other↝,
1144- CHr,    8-bromo-7-methoxychrysin-induced apoptosis of hepatocellular carcinoma cells involves ROS and JNK
- in-vitro, HCC, HepG2 - in-vitro, HCC, Bel-7402 - in-vitro, Nor, HL7702
Casp3↑, *ROS∅, ROS↑, JNK↑, *toxicity↓,
1585- Citrate,    Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S - in-vitro, Nor, HEK293
Apoptosis↑, Ferroptosis↑, Ca+2↓, CaMKII ↓, Akt↓, mTOR↓, Hif1a↓, ROS↑, ChemoSen↑, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, Cyt‑c↑, GlucoseCon↓, lactateProd↓, Pyruv↓, GLUT1↓, HK2↓, PFKP↓, Glycolysis↓, Hif1a↓, p‑Akt↓, p‑mTOR↓, Iron↑, lipid-P↑, MDA↑, ROS↑, H2O2↑, mtDam↑, GSH↓, GPx↓, GPx4↓, NADPH/NADP+↓, eff↓, FTH1↓, LC3‑Ⅱ/LC3‑Ⅰ↑, NCOA4↑, eff↓, TumCG↓,
4764- CoQ10,  VitE,    Auxiliary effect of trolox on coenzyme Q10 restricts angiogenesis and proliferation of retinoblastoma cells via the ERK/Akt pathway
- in-vitro, RPE, Y79 - in-vitro, Nor, ARPE-19 - in-vivo, NA, NA
tumCV↓, Apoptosis↑, ROS↑, MMP↓, TumCCA↑, VEGF↓, ERK↓, Akt↓, ChemoSen↑, chemoP↑, toxicity↓, angioG↓,
1864- DCA,  MET,    Dichloroacetate Enhances Apoptotic Cell Death via Oxidative Damage and Attenuates Lactate Production in Metformin-Treated Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D - in-vitro, Nor, MCF10
PDKs↓, eff↑, ROS↑, PDK1↓, lactateProd↓, p‑PDH↑, Dose∅, OCR↑, DNA-PK↑, γH2AX↑, cl‑PARP↑, selectivity↑, *toxicity∅,
2272- dietMet,    Methionine restriction - Association with redox homeostasis and implications on aging and diseases
- Review, Nor, NA
*OS↑, *mt-ROS↓, *H2S↑, *FGF21↑, *cognitive↑, *GutMicro↑, *IGF-1↓, *mTOR↓, *GSH↑, *SOD↑, *MDA↓, *NRF2↑, *HO-1↑, *NQO1↑, *GLUT4↑, *Glycolysis↑, *HK2↑, *PFK↑, *PKM2↑, *GlucoseCon↑, *ATF4↑, *PPARα↑, GSH↓, GSTs↑, ROS↑, *neuroP↑,

Showing Research Papers: 1 to 50 of 112
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 112

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   compI↓, 1,   Fenton↑, 1,   Ferroptosis↑, 4,   GPx↓, 3,   GPx4↓, 2,   GSH↓, 7,   GSH/GSSG↓, 1,   GSSG↑, 1,   GSTs↑, 1,   H2O2↑, 1,   HO-1↓, 1,   Iron↑, 3,   i-Iron↑, 1,   Keap1↑, 1,   lipid-P↑, 3,   MDA↑, 4,   NADH↓, 1,   NADPH/NADP+↓, 1,   NRF2↓, 1,   NRF2↑, 1,   OXPHOS↓, 3,   PARK2↑, 1,   RNS↑, 1,   ROS↑, 39,   ROS⇅, 1,   i-ROS↑, 1,   mt-ROS↑, 4,   SOD↓, 1,   Thiols↓, 1,   TrxR↓, 1,   mt-TrxR1↓, 1,   mt-TrxR2↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 2,   NCOA4↑, 2,   Tf↑, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 3,   ATP∅, 1,   compIII↓, 1,   compIII↑, 1,   ETC↓, 1,   MEK↓, 1,   mitResp↓, 1,   MMP↓, 13,   MPT↑, 1,   mtDam↑, 1,   OCR↑, 1,   p42↑, 1,   PINK1↑, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   AMPK↑, 3,   p‑AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 2,   lactateProd↓, 2,   LDH?, 1,   LDH↑, 1,   NADPH↝, 1,   p‑PDH↑, 1,   PDK1↓, 1,   PDKs↓, 1,   PFKP↓, 1,   Pyruv↓, 1,   p‑S6K↓, 1,   SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 15,   Bak↑, 2,   BAX↑, 10,   Bax:Bcl2↑, 1,   Bcl-2↓, 11,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 3,   Casp3↑, 11,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 9,   Cyt‑c↑, 11,   DR5↑, 2,   Ferroptosis↑, 4,   JNK↑, 2,   p‑JNK↑, 1,   MLKL↑, 1,   p‑MLKL↓, 1,   Necroptosis↑, 1,   p27↑, 1,   p38↑, 2,   p‑p38↓, 1,   p‑p38↑, 1,   Paraptosis↑, 2,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 4,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↝, 2,   tumCV↓, 7,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   p‑eIF2α↓, 1,   ER Stress↑, 6,   GRP78/BiP↓, 1,   HSP70/HSPA5↑, 1,   IRE1↑, 1,   UPR↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   BNIP3?, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 2,   LC3B↑, 1,   LC3II↑, 1,   p62↓, 2,   p62↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNA-PK↑, 1,   DNAdam↑, 7,   P53↑, 2,   p‑P53↑, 1,   PARP↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 4,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   cycE/CCNE↑, 1,   P21↑, 1,   TumCCA↑, 10,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CD133↓, 1,   cFos↑, 1,   CSCs↓, 1,   Diff↓, 1,   EMT↓, 2,   ERK↓, 2,   HDAC↓, 1,   mTOR↓, 3,   mTOR↑, 1,   p‑mTOR↓, 1,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,   TOP1↓, 1,   TOP2↓, 1,   TumCG?, 1,   TumCG↓, 5,   TumCG↑, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↓, 1,   Ca+2↑, 3,   E-cadherin↑, 1,   miR-139-5p↑, 1,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin↓, 1,   RIP3↑, 1,   p‑RIP3↑, 1,   Snail↓, 1,   TRIB3↑, 1,   TumCI?, 1,   TumCI↓, 4,   TumCMig↓, 5,   TumCP↓, 4,   TumCP↑, 1,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   EPR↑, 1,   Hif1a↓, 6,   Hif1a↑, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   GLUT1↑, 1,  

Immune & Inflammatory Signaling ⓘ

CCR7↓, 1,   COX2↓, 1,   CXCR4↓, 1,   IKKα↓, 1,   IL6↓, 1,   Inflam↓, 1,   JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   PGE2↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↝, 2,   BioEnh↑, 2,   ChemoSen↑, 4,   ChemoSen∅, 1,   Dose?, 1,   Dose↓, 2,   Dose↑, 1,   Dose↝, 3,   Dose∅, 2,   eff↓, 11,   eff↑, 14,   eff↝, 1,   P450↓, 1,   RadioS↑, 2,   selectivity↓, 2,   selectivity↑, 25,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   IL6↓, 1,   LDH?, 1,   LDH↑, 1,   TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   AntiTum↑, 3,   chemoP↑, 3,   chemoPv↑, 1,   neuroP↑, 1,   Obesity↓, 1,   RenoP↑, 1,   toxicity↓, 1,   toxicity↝, 2,   TumVol↓, 2,   TumW↓, 3,   Weight↑, 1,  
Total Targets: 236

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

TMAO↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 2,   GSH↓, 1,   GSH↑, 1,   GSR↑, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 2,   MDA↑, 1,   NQO1↑, 1,   NRF2↑, 2,   NRF2↝, 1,   ROS↓, 5,   ROS↑, 8,   ROS⇅, 1,   ROS∅, 9,   mt-ROS↓, 1,   mt-ROS↑, 1,   SOD↑, 2,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   Insulin↑, 1,   MMP↓, 1,   MMP∅, 1,   UCP1↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   FGF21↑, 1,   glucose↓, 1,   GlucoseCon↑, 2,   Glycolysis↑, 2,   H2S↑, 1,   HK2↑, 1,   NADPH↑, 1,   PFK↑, 1,   PKM2↑, 1,   PPARα↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   iNOS↓, 1,   JNK↑, 1,   TRPV1↑, 2,  

Transcription & Epigenetics ⓘ

other↑, 1,   other↝, 3,  

Protein Folding & ER Stress ⓘ

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

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration ⓘ

AntiAg↓, 1,   AntiAg↑, 2,   Ca+2↑, 2,   CLDN1↓, 1,   TJ↓, 1,   TumCP↓, 1,   ZO-1↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   Inflam↓, 2,   Inflam↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 1,   BioAv↝, 1,   Dose?, 1,   Dose↝, 2,   eff↓, 1,   eff↑, 3,   Half-Life↓, 2,  

Clinical Biomarkers ⓘ

BP↓, 1,   GutMicro↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 2,   cognitive↓, 2,   cognitive↑, 1,   hepatoP↑, 1,   neuroP↑, 3,   Obesity↓, 1,   OS↑, 2,   Pain↓, 2,   RenoP↑, 1,   toxicity↓, 11,   toxicity↝, 1,   toxicity∅, 4,  

Infection & Microbiome ⓘ

AntiViral↑, 1,   Bacteria↓, 2,  
Total Targets: 103

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
12 Silver-NanoParticles
11 Magnetic Fields
5 Quercetin
4 doxorubicin
4 Ashwagandha(Withaferin A)
4 Shikonin
3 Radiotherapy/Radiation
3 Allicin (mainly Garlic)
3 Apigenin (mainly Parsley)
3 Baicalein
3 Boswellia (frankincense)
3 Capsaicin
3 EGCG (Epigallocatechin Gallate)
3 Parthenolide
3 Sulforaphane (mainly Broccoli)
2 Vitamin C (Ascorbic Acid)
2 Alpha-Lipoic-Acid
2 Cisplatin
2 Metformin
2 Berberine
2 Lycopene
2 Carvacrol
2 Emodin
2 Honokiol
2 Hyperthermia
2 Phenylbutyrate
2 Propolis -bee glue
2 Propyl gallate
2 Piperlongumine
2 Plumbagin
2 Selenium NanoParticles
2 Selenite (Sodium)
2 Thymoquinone
1 3-bromopyruvate
1 Auranofin
1 Artemisinin
1 Betulinic acid
1 beta-carotene(VitA)
1 Butyrate
1 Chlorogenic acid
1 Curcumin
1 Resveratrol
1 Choline
1 Chrysin
1 Citric Acid
1 Coenzyme Q10
1 Vitamin E
1 Dichloroacetate
1 diet Methionine-Restricted Diet
1 diet Short Term Fasting
1 Ellagic acid
1 Chemotherapy
1 Electrical Pulses
1 Garcinol
1 Hydroxycinnamic-acid
1 HydroxyTyrosol
1 Methylene blue
1 Magnetic Field Rotating
1 SonoDynamic Therapy UltraSound
1 Phenethyl isothiocyanate
1 Copper and Cu NanoParticles
1 EMF
1 Rosmarinic acid
1 chitosan
1 Vitamin K2
1 Zinc
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:49  Cells:%  prod#:%  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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