ROS Cancer Research Results

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

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

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

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

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

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

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

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

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




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



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






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






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






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






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






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






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






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






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






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






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






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






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






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






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






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






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






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






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






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






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






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






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






ROS">Piperine
+±[D][F]ROS-secondary






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






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






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






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






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
2633- Api,    Apigenin induces ROS-dependent apoptosis and ER stress in human endometriosis cells
- in-vitro, EC, NA
TumCP↓, TumCCA↑, MMP↓, Ca+2↑, BAX↑, Cyt‑c↑, ROS↑, lipid-P↑, ER Stress↑, UPR↑, p‑ERK↓, ERK↓, JNK↑,
2634- Api,    Apigenin induces both intrinsic and extrinsic pathways of apoptosis in human colon carcinoma HCT-116 cells
- in-vitro, CRC, HCT116
TumCG↓, TumCCA↑, MMP↓, ROS↑, Ca+2↑, ER Stress↑, mtDam↑, CHOP↑, DR5↑, cl‑BID↑, BAX↑, Cyt‑c↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, Apoptosis↑,
2637- Api,    Apigenin Alleviates Endoplasmic Reticulum Stress-Mediated Apoptosis in INS-1 β-Cells
- in-vitro, Diabetic, NA
*other↝, *Insulin↑, ER Stress↓, *CHOP↓, *cl‑Casp3↓, *ROS↓, *Inflam↓, *TXNIP↓,
2638- Api,    Apigenin, by activating p53 and inhibiting STAT3, modulates the balance between pro-apoptotic and pro-survival pathways to induce PEL cell death
- in-vitro, lymphoma, PEL
TumCD↑, TumAuto↑, ROS↓, P53↑, Catalase↑, STAT3↓,
2639- Api,    Plant flavone apigenin: An emerging anticancer agent
- Review, Var, NA
*antiOx↑, *Inflam↓, AntiCan↑, ChemoSen↑, BioEnh↑, chemoPv↑, IL6↓, STAT3↓, NF-kB↓, IL8↓, eff↝, Akt↓, PI3K↓, HER2/EBBR2↓, cycD1/CCND1↓, CycD3↓, p27↑, FOXO3↑, STAT3↓, MMP2↓, MMP9↓, VEGF↓, Twist↓, MMP↓, ROS↑, NADPH↑, NRF2↓, SOD↓, COX2↓, p38↑, Telomerase↓, HDAC↓, HDAC1↓, HDAC3↓, Hif1a↓, angioG↓, uPA↓, Ca+2↑, Bax:Bcl2↑, Cyt‑c↑, Casp9↑, Casp12↑, Casp3↑, cl‑PARP↑, E-cadherin↑, β-catenin/ZEB1↓, cMyc↓, CDK4↓, CDK2↓, CDK6↓, IGF-1↓, CK2↓, CSCs↓, FAK↓, Gli↓, GLUT1↓,
2640- Api,    Apigenin: A Promising Molecule for Cancer Prevention
- Review, Var, NA
chemoPv↑, ITGB4↓, TumCI↓, TumMeta↓, Akt↓, ERK↓, p‑JNK↓, *Inflam↓, *PKCδ↓, *MAPK↓, EGFR↓, CK2↓, TumCCA↑, CDK1↓, P53↓, P21↑, Bax:Bcl2↑, Cyt‑c↑, APAF1↑, Casp↑, cl‑PARP↑, VEGF↓, Hif1a↓, IGF-1↓, IGFBP3↑, E-cadherin↑, β-catenin/ZEB1↓, HSPs↓, Telomerase↓, FASN↓, MMPs↓, HER2/EBBR2↓, CK2↓, eff↑, AntiAg↑, eff↑, FAK↓, ROS↑, Bcl-2↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp7↑, cl‑Casp8↑, cl‑Casp9↑, cl‑IAP2↑, AR↓, PSA↓, p‑pRB↓, p‑GSK‐3β↓, CDK4↓, ChemoSen↑, Ca+2↑, cal2↑,
2593- Api,    Apigenin promotes apoptosis of 4T1 cells through PI3K/AKT/Nrf2 pathway and improves tumor immune microenvironment in vivo
- in-vivo, BC, 4T1
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, MMP↑, ROS↑, p‑PI3K↓, PI3K↓, Akt↓, NRF2↓, AntiTum↑, OS↑,
2583- Api,  Rad,    The influence of apigenin on cellular responses to radiation: From protection to sensitization
- Review, Var, NA
radioP↑, RadioS↑, *COX2↓, *ROS↓, VEGF↓, MMP2↓, STAT3↓, AMPK↑, Apoptosis↑, MMP9↓, glucose↓,
2318- Api,    Apigenin as a multifaceted antifibrotic agent: Therapeutic potential across organ systems
- Review, Nor, NA
*ROS↓, *PKM2↓, *Hif1a↓, *TGF-β↓, *AMPK↑, *Inflam↓, *PI3K↓, *Akt↑, *NRF2↑, *NF-kB↓,
2317- Api,    Apigenin intervenes in liver fibrosis by regulating PKM2-HIF-1α mediated oxidative stress
- in-vivo, Nor, NA
*hepatoP↑, *PKM2↓, *Hif1a↓, *MDA↓, *Catalase↓, *GSH↑, *SOD↑, *GPx↑, *TAC↑, *α-SMA↓, *Vim↓, *ROS↓,
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↓,
1547- Api,    Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading
- Review, NA, NA
angioG↓, EMT↓, CSCs↓, TumCCA↑, Dose∅, ROS↑, MMP↓, Catalase↓, GSH↓, PI3K↓, Akt↓, NF-kB↓, OCT4↓, Nanog↓, SIRT3↓, SIRT6↓, eff↑, eff↑, Cyt‑c↑, Bax:Bcl2↑, p‑GSK‐3β↓, FOXO3↑, p‑STAT3↓, MMP2↓, MMP9↓, COX2↓, MMPs↓, NRF2↓, HDAC↓, Telomerase↓, eff↑, eff↑, eff↑, eff↑, eff↑, XIAP↓, survivin↓, CK2↓, HSP90↓, Hif1a↓, FAK↓, EMT↓,
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↓,
1537- Api,    Apigenin as Tumor Suppressor in Cancers: Biotherapeutic Activity, Nanodelivery, and Mechanisms With Emphasis on Pancreatic Cancer
- Review, PC, NA
TumCP↓, TumCCA↑, Apoptosis↑, MMPs↓, Akt↓, *BioAv↑, *BioAv↓, Half-Life∅, Hif1a↓, GLUT1↓, VEGF↓, ChemoSen↑, ROS↑, Bcl-2↓, Bcl-xL↓, BAX↑, BIM↑,
1536- Api,    Apigenin causes necroptosis by inducing ROS accumulation, mitochondrial dysfunction, and ATP depletion in malignant mesothelioma cells
- in-vitro, MM, MSTO-211H - in-vitro, MM, H2452
tumCV↓, ROS↑, MMP↓, ATP↓, Apoptosis↑, Necroptosis↑, DNAdam↑, TumCCA↑, Casp3↑, cl‑PARP↑, MLKL↑, p‑RIP3↑, Bax:Bcl2↑, eff↓, eff↓,
1564- Api,    Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation
- in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
MDM2↓, NF-kB↓, p65↓, P21↑, ROS↑, GSH↓, MMP↓, Cyt‑c↑, Apoptosis↑, P53↑, eff↓, Bcl-xL↓, Bcl-2↓, BAX↑, Casp↑, TumCG↓, TumVol↓, TumW↓,
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↓,
3887- Api,    The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice
- in-vivo, AD, NA
*Inflam↓, *ROS↓, *Aβ↓, *memory↑, *AChE↓, *Ach↑, *Dose↑, *BDNF↑, *TrkB↑, *p‑CREB↑, *BBB↑, *Ca+2?,
3884- Api,    Neuroprotective, Anti-Amyloidogenic and Neurotrophic Effects of Apigenin in an Alzheimer’s Disease Mouse Model
- in-vivo, AD, NA
*memory↑, *Aβ↓, *BACE↓, *antiOx↑, *BDNF↑, *p‑CREB↑, *p‑ERK↑, *ROS↓, *SOD↑, *GPx↑, *neuroP↑,
3817- Aroma,    Therapeutic potential of aromatic plant extracts in Alzheimer's disease: Comprehensive review of their underlying mechanisms
- Review, AD, NA
*BChE↓, *AChE↓, *other↓, *other?, *Ach?, *eff↑, *antiOx↑, *ROS↓, *cognitive↑, *Mood↑, *Sleep↑,
3821- Aroma,    Neuroprotective and Anti-Aging Potentials of Essential Oils from Aromatic and Medicinal Plants
- Review, AD, NA
*cognitive↑, *AChE↓, *BChE↓, *ROS↓, *other↓, *other↓, *other↓, *other↓, *other↓, *memory↑, *BACE↓, *Mood↑, *motorD↑,
3382- ART/DHA,    Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?
- Review, Var, NA
AntiCan↑, toxicity↑, Ferroptosis↑, ROS↑, TumCCA↑, BioAv↝, eff↝, Half-Life↓, Ferritin↓, GPx4↓, NADPH↓, GSH↓, BAX↑, Cyt‑c↑, cl‑Casp3↑, VEGF↓, IL8↓, COX2↓, MMP9↓, E-cadherin↑, MMP2↓, NF-kB↓, p16↑, CDK4↓, cycD1/CCND1↓, p62↓, LC3II↑, EMT↓, CSCs↓, Wnt↓, β-catenin/ZEB1↓, uPA↓, TumAuto↑, angioG↓, ChemoSen↑,
3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, Apoptosis↑, TumMeta↓, angioG↓, TumAuto↑, ER Stress↑, ROS↑, Ca+2↑, p38↑, HSP70/HSPA5↓, PPARγ↑, GLUT1↓, Glycolysis↓, PI3K↓, Akt↓, Hif1a↓, PKM2↓, lactateProd↓, GlucoseCon↓, EMT↓, Slug↓, Zeb1↓, ZEB2↓, Twist↓, Snail?, CAFs/TAFs↓, TGF-β↓, p‑STAT3↓, M2 MC↓, uPA↓, HH↓, AXL↓, VEGFR2↓, JNK↑, Beclin-1↑, GRP78/BiP↑, eff↑, eff↑, eff↑, eff↑, eff↑, eff↑, IL4↓, DR5↑, Cyt‑c↑, Fas↑, FADD↑, cl‑PARP↑, cycE/CCNE↓, CDK2↓, CDK4↓, Mcl-1↓, Ki-67↓, Bcl-2↓, CDK6↓, VEGF↓, COX2↓, MMP9↓,
3384- ART/DHA,    Dihydroartemisinin triggers ferroptosis in primary liver cancer cells by promoting and unfolded protein response‑induced upregulation of CHAC1 expression
- in-vitro, Liver, Hep3B - in-vitro, Liver, HUH7 - in-vitro, Liver, HepG2
Ferroptosis↑, ROS↑, GSH↓, UPR↑, GPx4↓, PERK↑, eIF2α↑, ATF4↑,
3387- ART/DHA,    Ferroptosis: A New Research Direction of Artemisinin and Its Derivatives in Anti-Cancer Treatment
- Review, Var, NA
BioAv↓, lipid-P↑, Ferroptosis↑, Iron↑, GPx4↓, GSH↓, P53↑, ER Stress↑, PERK↑, ATF4↑, GRP78/BiP↑, CHOP↑, ROS↑, NRF2↑,
3388- ART/DHA,    Keap1 Cystenine 151 as a Potential Target for Artemisitene-Induced Nrf2 Activation
- in-vitro, Lung, A549 - in-vitro, Nor, GP-293 - in-vitro, BC, MDA-MB-231
NRF2↑, ROS∅,
3389- ART/DHA,    Emerging mechanisms and applications of ferroptosis in the treatment of resistant cancers
- Review, Var, NA
GSH↓, ROS↑, NRF2↑, eff↑,
3390- ART/DHA,    Ferroptosis: The Silver Lining of Cancer Therapy
Ferroptosis↑, Iron↑, NCOA4↝, ROS↑, Fenton↑, Tf↓,
3345- ART/DHA,    Dihydroartemisinin-induced unfolded protein response feedback attenuates ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells
- in-vitro, GBM, NA
ROS↑, Ferroptosis↑, lipid-P↑, HSP70/HSPA5↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MDA↑, GSH↓, eff↑, GPx4↑,
3391- ART/DHA,    Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug
- Review, Var, NA
TumCP↓, TumMeta↓, angioG↓, TumVol↓, BioAv↓, Half-Life↓, BioAv↑, eff↑, eff↓, ROS↑, selectivity↑, TumCCA↑, survivin↓, BAX↑, Casp3↓, Casp8↑, Casp9↑, CDC25↓, CycB/CCNB1↓, NF-kB↓, cycD1/CCND1↓, cycE/CCNE↓, E2Fs↓, P21↑, p27↑, ADP:ATP↑, MDM2↓, VEGF↓, IL8↓, COX2↓, MMP9↓, ER Stress↓, cMyc↓, GRP78/BiP↑, DNAdam↑, AP-1↓, MMP2↓, PKCδ↓, Raf↓, ERK↓, JNK↓, PCNA↓, CDK2↓, CDK4↓, TOP2↓, uPA↓, MMP7↓, TIMP2↑, Cdc42↑, E-cadherin↑,
3392- ART/DHA,    Artemisinin inhibits inflammatory response via regulating NF-κB and MAPK signaling pathways
- in-vitro, Nor, Hep3B - in-vivo, NA, NA
*Inflam↓, *NF-kB↓, *ROS↓, *p‑p38↓, *p‑ERK↓,
3393- ART/DHA,    Artemisinin-derived artemisitene blocks ROS-mediated NLRP3 inflammasome and alleviates ulcerative colitis
- in-vivo, Col, NA
*ROS↓, *NLRP3↓, *Inflam↓,
3396- ART/DHA,    Progress on the study of the anticancer effects of artesunate
- Review, Var, NA
TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, Diff↑, TumAuto↑, angioG↓, TumCCA↑, ROS↑, AMPK↑, mTOR↑, ChemoSen↑, Tf↑, Ferroptosis↑, Ferritin↓, lipid-P↑, CDK1↑, CDK2↑, CDK4↑, CDK6↑, SIRT1↑, COX2↓, IL1β↓, survivin↓, DNAdam↑, RadioS↑,
3666- ART/DHA,    Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling
- NA, AD, NA
*Inflam↓, *neuroP↑, *TLR4↓, *NF-kB↓, *memory↑, *ROS↓, *iNOS↓, *COX2↓, *cognitive↑,
3667- ART/DHA,    Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia
- Review, Sepsis, NA
*cognitive↑, *neuroP↑, *TNF-α↓, *IL6↓, *NF-kB↓, *AMPK↑, *ROS↓, *Akt↑, *MCP1↓, *MIP2↓, *TGF-β↑, *Inflam↓,
575- ART/DHA,    Dihydroartemisinin initiates ferroptosis in glioblastoma through GPX4 inhibition
- in-vitro, GBM, U87MG
GPx4↓, xCT∅, ROS↑, Ferroptosis↑, ACSL4∅,
571- ART/DHA,  TMZ,    Artesunate enhances the therapeutic response of glioma cells to temozolomide by inhibition of homologous recombination and senescence
- vitro+vivo, GBM, A172 - vitro+vivo, GBM, U87MG
HR↓, RAD51↓, Apoptosis↑, necrosis↑, ROS↑, ChemoSen↑,
556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
IL6↓, IL1↓, TNF-α↓, TGF-β↓, NF-kB↓, MIP2↓, PGE2↓, NO↓, Hif1a↓, KDR/FLK-1↓, VEGF↓, MMP2↓, TIMP2↑, ITGB1↑, NCAM↑, p‑ATM↑, p‑ATR↑, p‑CHK1↑, p‑Chk2↑, Wnt/(β-catenin)↓, PI3K↓, Akt↓, ERK↓, cMyc↓, mTOR↓, survivin↓, cMET↓, EGFR↓, cycD1/CCND1↓, cycE1↓, CDK4/6↓, p16↑, p27↑, Apoptosis↑, TumAuto↑, Ferroptosis↑, oncosis↑, TumCCA↑, ROS↑, DNAdam↑, RAD51↓, HR↓,
558- ART/DHA,    Artemisinin and Its Synthetic Derivatives as a Possible Therapy for Cancer
- Review, NA, NA
ROS↑, oncosis↑, Apoptosis↑, LysoPr↑, TumAuto↑, Wnt/(β-catenin)↑, AMP↓, NF-kB↓, Myc↓, CREBBP↓, mTOR↓, E-cadherin↑,
559- ART/DHA,    Artemisinin and its derivatives: a promising cancer therapy
- Review, NA, NA
ROS↑,
566- ART/DHA,  2DG,    Dihydroartemisinin inhibits glucose uptake and cooperates with glycolysis inhibitor to induce apoptosis in non-small cell lung carcinoma cells
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
GlucoseCon↓, ATP↓, lactateProd↓, p‑S6↓, mTOR↓, GLUT1↓, Casp9↑, Casp8↑, Casp3↑, Cyt‑c↑, AIF↑, ROS↑,
1076- ART/DHA,    The Potential Mechanisms by which Artemisinin and Its Derivatives Induce Ferroptosis in the Treatment of Cancer
- Review, NA, NA
Ferroptosis↑, ROS↑, ER Stress↑, i-Iron↓, TumAuto↑, AMPK↑, mTOR↑, P70S6K↑, Fenton↑, lipid-P↑, ROS↑, ChemoSen↑, NRF2↑, NRF2↓,
1026- ART/DHA,    Artemisinin improves the efficiency of anti-PD-L1 therapy in T-cell lymphoma
Ferroptosis↑, ROS↑, ERK↓, PD-L1↓,
5380- ART/DHA,    Artemisinin and Its Derivatives as Potential Anticancer Agents
- Review, Var, NA
TumCG↓, angioG↓, Ferroptosis↑, TumCP↑, TumAuto↑, CSCs↑, eff↑, YAP/TEAD↓, TumCCA↑, ROS↑, ChemoSen↑, N-cadherin↓, Vim↓, MMP9↓, eff↑, STAT3↓, CD133↓, CD44↓, Nanog↓, cMyc↓, OCT4↓, Akt↓, mTOR↓,
5379- ART/DHA,    Iron-fueled ferroptosis: a new axis for immunomodulation to overcome cancer drug resistance—from immune microenvironment crosstalk to therapeutic translation
Ferritin↓, Iron↑, Fenton↑, lipid-P↑, ChemoSen↑, ROS↑, eff↝,
5378- ART/DHA,    Natural Agents Modulating Ferroptosis in Cancer: Molecular Pathways and Therapeutic Perspectives
- Review, Var, NA
Ferroptosis↑, Iron↑, lipid-P↑, MOMP↑, AntiCan↑, NCOA4↑, GSH↓, GPx4↓, ROS↑, ChemoSen↑, ER Stress↑, DNAdam↑, angioG↓, TumCCA↑, eff↓,
5376- ART/DHA,    Artemisinin compounds sensitize cancer cells to ferroptosis by regulating iron homeostasis
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, CRC, SW48 - in-vitro, BC, MDA-MB-453
Ferroptosis↑, Ferritin↓, Iron↑, eff↑, TumAuto↑, LC3II↑, ROS↑,
5137- ART/DHA,    Autophagy-dependent cell cycle arrest in esophageal cancer cells exposed to dihydroartemisinin
- vitro+vivo, ESCC, Eca109
tumCV↓, TumCCA↑, ROS↑, TumAuto↑, eff↓, TRF2↓, TumCP↓,
5133- ART/DHA,    Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
AntiTum↑, tumCV↓, Apoptosis↓, MMP↓, Cyt‑c↑, Casp9↑, CHOP↑, GRP78/BiP↑, eIF2α↑, Casp12↑, ER Stress↑, TumAuto↑, ROS↑,
5132- ART/DHA,    Dihydroartemisinin Exerts Its Anticancer Activity through Depleting Cellular Iron via Transferrin Receptor-1
- in-vitro, Liver, HepG2 - in-vitro, BC, MCF7
Iron↓, TfR1/CD71↓, ROS↑,

Showing Research Papers: 251 to 300 of 2389
Prev Page 6 of 48 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2389

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Catalase↑, 1,   Fenton↑, 3,   Ferroptosis↑, 13,   GPx4↓, 5,   GPx4↑, 1,   GSH↓, 9,   Iron↓, 1,   Iron↑, 5,   i-Iron↓, 1,   lipid-P↑, 7,   MDA↑, 2,   NRF2↓, 4,   NRF2↑, 4,   ROS↓, 1,   ROS↑, 37,   ROS∅, 1,   SIRT3↓, 1,   SOD↓, 1,   xCT∅, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 4,   NCOA4↑, 1,   NCOA4↝, 1,   Tf↓, 1,   Tf↑, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↑, 1,   AIF↑, 2,   ATP↓, 2,   CDC25↓, 1,   MMP↓, 8,   MMP↑, 1,   mtDam↑, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4∅, 1,   AMP↓, 1,   AMPK↑, 3,   cMyc↓, 4,   FASN↓, 1,   glucose↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 1,   lactateProd↓, 2,   NADPH↓, 1,   NADPH↑, 1,   PKM2↓, 1,   PPARγ↑, 1,   p‑S6↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 9,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 13,   BAX↑, 7,   Bax:Bcl2↑, 4,   Bcl-2↓, 5,   Bcl-xL↓, 2,   cl‑BID↑, 1,   BIM↑, 2,   Casp↑, 2,   Casp12↑, 2,   Casp3↓, 1,   Casp3↑, 4,   cl‑Casp3↑, 3,   cl‑Casp7↑, 1,   Casp8↑, 3,   cl‑Casp8↑, 2,   Casp9↑, 5,   cl‑Casp9↑, 2,   p‑Chk2↑, 1,   CK2↓, 4,   Cyt‑c↑, 13,   DR5↑, 2,   FADD↑, 1,   Fas↑, 1,   Ferroptosis↑, 13,   cl‑IAP2↑, 1,   JNK↓, 1,   JNK↑, 2,   p‑JNK↓, 1,   Mcl-1↓, 1,   MDM2↓, 2,   MLKL↑, 2,   p‑MLKL↓, 1,   MOMP↑, 1,   Myc↓, 1,   Necroptosis↑, 2,   necrosis↑, 1,   oncosis↑, 2,   p27↑, 3,   p38↑, 2,   survivin↓, 4,   Telomerase↓, 3,   TumCD↑, 1,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

p‑pRB↓, 1,   tumCV↓, 4,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 3,   eIF2α↑, 2,   ER Stress↓, 2,   ER Stress↑, 8,   GRP78/BiP↑, 5,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 1,   HSP90↓, 1,   HSPs↓, 1,   PERK↑, 2,   UPR↑, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 2,   p62↓, 1,   p62↑, 1,   TumAuto↑, 12,  

DNA Damage & Repair(tgid=10) ⓘ

p‑ATM↑, 1,   p‑ATR↑, 1,   p‑CHK1↑, 1,   DNAdam↑, 6,   HR↓, 2,   p16↑, 2,   P53↓, 1,   P53↑, 3,   p‑P53↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 4,   PCNA↓, 1,   RAD51↓, 2,   SIRT6↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK1↑, 1,   CDK2↓, 3,   CDK2↑, 1,   CDK4↓, 5,   CDK4↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   CycD3↓, 1,   cycE/CCNE↓, 2,   cycE1↓, 1,   E2Fs↓, 1,   P21↑, 3,   TumCCA↑, 13,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD133↓, 1,   CD44↓, 1,   cMET↓, 1,   CREBBP↓, 1,   CSCs↓, 3,   CSCs↑, 1,   Diff↑, 1,   EMT↓, 4,   ERK↓, 5,   p‑ERK↓, 1,   FOXO3↑, 2,   Gli↓, 1,   p‑GSK‐3β↓, 2,   HDAC↓, 2,   HDAC1↓, 1,   HDAC3↓, 1,   HH↓, 1,   IGF-1↓, 2,   IGFBP3↑, 1,   mTOR↓, 5,   mTOR↑, 2,   Nanog↓, 2,   OCT4↓, 2,   P70S6K↑, 1,   PI3K↓, 6,   p‑PI3K↓, 1,   STAT3↓, 5,   p‑STAT3↓, 2,   TOP2↓, 1,   TRF2↓, 1,   TumCG↓, 3,   TumCG↑, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,   Wnt/(β-catenin)↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   AP-1↓, 1,   AXL↓, 1,   Ca+2↑, 5,   CAFs/TAFs↓, 1,   cal2↑, 1,   Cdc42↑, 1,   CDK4/6↓, 1,   E-cadherin↑, 5,   FAK↓, 3,   ITGB1↑, 1,   ITGB4↓, 1,   Ki-67↓, 1,   LysoPr↑, 1,   MMP2↓, 6,   MMP7↓, 1,   MMP9↓, 7,   MMPs↓, 3,   N-cadherin↓, 1,   NCAM↑, 1,   PKCδ↓, 1,   RIP3↑, 1,   p‑RIP3↑, 2,   Slug↓, 1,   Snail?, 1,   TGF-β↓, 2,   TIMP2↑, 2,   TumCI↓, 4,   TumCMig↓, 3,   TumCP↓, 8,   TumCP↑, 1,   TumMeta↓, 3,   Twist↓, 2,   uPA↓, 4,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 8,   ATF4↑, 3,   EGFR↓, 2,   Hif1a↓, 6,   KDR/FLK-1↓, 1,   NO↓, 1,   VEGF↓, 8,   VEGFR2↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 4,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 6,   IL1↓, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 2,   IL8↓, 3,   M2 MC↓, 1,   MIP2↓, 1,   NF-kB↓, 7,   p65↓, 1,   PD-L1↓, 1,   PGE2↓, 1,   PSA↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,   CDK6↓, 2,   CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   BioEnh↑, 1,   ChemoSen↑, 10,   ChemoSen∅, 1,   Dose∅, 2,   eff↓, 7,   eff↑, 22,   eff↝, 3,   Half-Life↓, 2,   Half-Life∅, 1,   RadioS↑, 2,   selectivity↓, 1,   selectivity↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   EGFR↓, 2,   Ferritin↓, 4,   HER2/EBBR2↓, 2,   IL6↓, 2,   Ki-67↓, 1,   Myc↓, 1,   PD-L1↓, 1,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   AntiTum↑, 2,   chemoP↑, 1,   chemoPv↑, 2,   neuroP↑, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↑, 1,   TumVol↓, 2,   TumW↓, 2,  
Total Targets: 278

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 4,   Catalase↓, 1,   GPx↑, 2,   GSH↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 12,   ROS∅, 1,   SOD↑, 2,   TAC↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

Insulin↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   p‑CREB↑, 2,   PKM2↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   cl‑Casp3↓, 1,   iNOS↓, 1,   MAPK↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach?, 1,   Ach↑, 1,   other?, 1,   other↓, 6,   other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

p‑ERK↓, 1,   p‑ERK↑, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

Ca+2?, 1,   PKCδ↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   TXNIP↓, 1,   Vim↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 2,   IL6↓, 1,   Inflam↓, 9,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 4,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3,   BChE↓, 2,   BDNF↑, 2,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,   BACE↓, 2,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 4,   hepatoP↑, 1,   memory↑, 4,   Mood↑, 2,   motorD↑, 1,   neuroP↑, 3,   Sleep↑, 1,   toxicity↓, 1,  
Total Targets: 65

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
122 Silver-NanoParticles
99 Curcumin
94 Quercetin
88 Magnetic Fields
74 Thymoquinone
56 Resveratrol
55 Shikonin
54 Vitamin C (Ascorbic Acid)
50 Berberine
50 Sulforaphane (mainly Broccoli)
49 Radiotherapy/Radiation
47 Lycopene
45 EGCG (Epigallocatechin Gallate)
43 Baicalein
42 Alpha-Lipoic-Acid
40 Selenite (Sodium)
40 Ashwagandha(Withaferin A)
40 Piperlongumine
39 Selenium NanoParticles
38 Artemisinin
37 Betulinic acid
36 Hydrogen Gas
34 Rosmarinic acid
33 Capsaicin
32 Silymarin (Milk Thistle) silibinin
29 Propolis -bee glue
29 Fisetin
28 Copper and Cu NanoParticles
28 Apigenin (mainly Parsley)
27 Chemotherapy
27 Honokiol
26 Allicin (mainly Garlic)
25 doxorubicin
25 Phenethyl isothiocyanate
24 Luteolin
24 Magnetic Field Rotating
23 Chrysin
22 Cisplatin
22 Vitamin K2
21 Chlorogenic acid
21 Gambogic Acid
20 Coenzyme Q10
20 chitosan
20 Juglone
18 Boron
17 salinomycin
17 Parthenolide
16 Emodin
16 Urolithin
15 Ellagic acid
15 Eugenol
14 Photodynamic Therapy
14 Auranofin
14 Boswellia (frankincense)
14 Carnosic acid
14 Carvacrol
14 Selenium
14 Crocetin
14 Phenylbutyrate
13 Dichloroacetate
13 Dandelion Root
13 Pterostilbene
12 Melatonin
12 Caffeic acid
12 VitK3,menadione
11 5-fluorouracil
11 Astaxanthin
11 Cinnamon
11 Graviola
11 Piperine
10 Beta-Caryophyllene
10 α-Bisabolol / Chamomile oil
10 Ursolic acid
10 diet FMD Fasting Mimicking Diet
10 Ferulic acid
10 Plumbagin
10 Nimbolide
9 SonoDynamic Therapy UltraSound
9 Andrographis
9 D-limonene
9 Bacopa monnieri
9 borneol
9 Centella asiatica / Gotu kola → asiaticoside
9 Diclofenac
8 Hydroxycinnamic-acid
8 Disulfiram
8 Electrical Pulses
8 Sulfasalazine
8 Hyperthermia
8 Methylene blue
8 Moringa oleifera
8 Propyl gallate
7 3-bromopyruvate
7 Gemcitabine (Gemzar)
7 EMF
7 Gold NanoParticles
7 Metformin
7 immunotherapy
7 Berbamine
7 brusatol
7 Carnosine
7 Celastrol
7 diet Methionine-Restricted Diet
7 eicosapentaenoic acid
7 HydroxyTyrosol
6 2-DeoxyGlucose
6 Anethole/trans-Anethole
6 Docetaxel
6 Biochanin A
6 Butyrate
6 Chlorophyllin
6 Citric Acid
6 Carvone
6 Aflavin-3,3′-digallate
5 1,8-Cineole
5 Brucea javanica
5 Bromelain
5 erastin
5 Thymol-Thymus vulgaris
5 Chocolate
5 Cichoric acid / Chicoric acid
5 Spermidine
5 Huperzine A/Huperzia serrata
5 Date Fruit Extract
5 Docosahexaenoic Acid
5 Garcinol
5 HydroxyCitric Acid
5 Magnolol
5 nicotinamide adenine dinucleotide
5 Rutin
4 chemodynamic therapy
4 Zinc
4 Vitamin E
4 Cucurbitacin
4 diet Short Term Fasting
4 Geraniol
4 γ-linolenic acid (Borage Oil)
4 Linalool
4 Magnesium
4 Naringin
4 Taurine
3 5-Aminolevulinic acid
3 Anthocyanins
3 Glucose
3 temozolomide
3 Black phosphorus
3 Paclitaxel
3 Catechins
3 Choline
3 Dihydrocaffeic Acid
3 Oxygen, Hyperbaric
3 Shilajit/Fulvic Acid
3 Ginkgo biloba
3 Orlistat
3 MCToil
3 Methylsulfonylmethane
3 Mushroom Lion’s Mane
3 Oleuropein
3 α-Santalol/Sandalwood oil
3 Shankhpushpi
3 Terpinen-4-ol / Tea Tree Oil
3 Turmerones
3 Vitamin B1/Thiamine
2 5-Hydroxytryptophan
2 Astragalus
2 DTS(dibenzyl trisulphide) from Anamu
2 Fennel Oil/Foeniculum vulgare
2 Aromatherapy
2 Ascorbyl Palmitate
2 Atorvastatin
2 Aloe anthraquinones
2 beta-glucans
2 Baicalin
2 xanthohumol
2 Cannabidiol
2 beta-carotene(VitA)
2 Bufalin/Huachansu
2 Bruteridin(bergamot juice)
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Cat’s Claw
2 Carica papaya leaf extract
2 Calorie Restriction Mimetics
2 Galantamine
2 CUSP9
2 Folic Acid, Vit B9
2 Fenbendazole
2 Galloflavin
2 Potassium
2 Methyl Jasmonate
2 Methylglyoxal
2 Myricetin
2 Vitamin B3,Niacin
2 Niclosamide (Niclocide)
2 Pachymic acid
2 Sanguinarine
2 Psoralidin
2 Radio Frequency
2 Sesame seeds and Oil
2 Iron
2 Salvia miltiorrhiza
2 Vitamin D3
1 cetuximab
1 entinostat
1 Camptothecin
1 Resiquimod
1 Anzaroot, Astragalus fasciculifolius Bioss
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 alpha Linolenic acid
1 Anti-oxidants
1 Sorafenib (brand name Nexavar)
1 tamoxifen
1 almonertinib
1 epirubicin
1 Lapatinib
1 Ras-selective lethal 3
1 Celecoxib
1 methotrexate
1 Aspirin
1 Rivastigmine
1 methylseleninic acid
1 Cyclopamine
1 Cysteamine
1 Dichloroacetophenone(2,2-)
1 Deguelin
1 diet Fermented Foods
1 diet Ketogenic
1 diet Plant based
1 Lemongrass Extract/Citral
1 Echinacea
1 Cannabichromene
1 Exercise
1 Fucoidan
1 Gallic acid
1 verapamil
1 hydroxychloroquine
1 Ginseng
1 hydrogen sulfide
1 Rapamycin
1 Ivermectin
1 lambertianic acid
1 Myrrh
1 N-Acetyl-Cysteine
1 No Product/Mechanism Only
1 Oleocanthal
1 sericin
1 Kaempferol
1 benzo(a)pyrene
1 Hyperoside
1 Perilla
1 Salvia officinalis
1 Oxaliplatin
1 Scoulerine
1 polyethylene glycol
1 acetaminophen
1 Formononetin
1 Silicic Acid
1 Squalene
1 Osimertinib
1 Adagrasib
1 Glutathione
1 statins
1 Safflower yellow
1 triptolide
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B2,Riboflavin
1 Vitamin B5,Pantothenic Acid
1 glucose deprivation
1 Transarterial Chemoembolization
1 probiotics
1 Zinc Oxide
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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