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


Lung, Lung Cancer: Click to Expand ⟱
Lung CSC (Cancer Stem Cells) markers (CD133, CD44, ALDHA1, Nanog and Oct4)
Scientific Papers found: Click to Expand⟱
3453- 5-ALA,    The heme precursor 5-aminolevulinic acid disrupts the Warburg effect in tumor cells and induces caspase-dependent apoptosis
- in-vitro, Lung, A549
OXPHOS↑, OCR↑, Warburg↓, ROS↑, SOD2↑, Catalase↑, HO-1↑, Casp3↑, Apoptosis↑,
5466- AF,    Auranofin Inhibition of Thioredoxin Reductase in a Preclinical Model of Small Cell Lung Cancer
- in-vivo, Lung, NA
TrxR↓, Dose↝, RadioS↑, ChemoSen↑, ROS↑, Diff↑, toxicity↓,
1908- AgNPs,    Exposure to Silver Nanoparticles Inhibits Selenoprotein Synthesis and the Activity of Thioredoxin Reductase
- in-vitro, Lung, A549
TrxR↓, TrxR1↓, ROS↑, ER Stress↑, TumCP↓, selenoP↓,
1903- AgNPs,    Novel Silver Complexes Based on Phosphanes and Ester Derivatives of Bis(pyrazol-1-yl)acetate Ligands Targeting TrxR: New Promising Chemotherapeutic Tools Relevant to SCLC Managemen
- in-vitro, Lung, U1285
TrxR↓, eff↝, ROS↑,
4414- AgNPs,    Silver nanoparticles: Forging a new frontline in lung cancer therapy
- Review, Lung, NA
tumCV↑, ROS↑, MMP↓, TumCCA↑, Apoptosis↑, angioG↓,
4380- AgNPs,    Silver nanoparticles induce toxicity in A549 cells via ROS-dependent and ROS-independent pathways
- in-vitro, Lung, A549
ROS↑, tumCV↓, MMP↓, TumCCA↑, PCNA↓, eff↓,
4383- AgNPs,    Exploring the Potentials of Silver Nanoparticles in Overcoming Cisplatin Resistance in Lung Adenocarcinoma: Insights from Proteomic and Xenograft Mice Studies
- in-vitro, Lung, A549 - in-vivo, Lung, A549
Apoptosis↑, VEGF↓, P53↓, TumCCA↑, ROS↑, AntiTum↑, eff↑, ATP↓, eff↑, CTR1↑,
4555- AgNPs,    Silver nanoparticles from Dendropanax morbifera Léveille inhibit cell migration, induce apoptosis, and increase generation of reactive oxygen species in A549 lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Liver, HepG2
*Bacteria↓, tumCV↓, selectivity↑, ROS↑, Apoptosis↑, TumCMig↓, AntiCan↑,
5147- AgNPs,    Size dependent anti-invasiveness of silver nanoparticles in lung cancer cells
- in-vitro, Lung, A549
TumCMig↓, TumCI↓, ROS↑, p‑NF-kB↑, selectivity↑, eff↝,
327- AgNPs,  MS-275,    Combination Effect of Silver Nanoparticles and Histone Deacetylases Inhibitor in Human Alveolar Basal Epithelial Cells
- in-vitro, Lung, A549
Apoptosis↑, ROS↑, LDH↓, TNF-α↑, mtDam↑, TumAuto↑, Casp3↑, Casp9↑, DNAdam↑,
371- AgNPs,    Cytotoxicity and genotoxicity of silver nanoparticles in the human lung cancer cell line, A549
- in-vitro, Lung, A549
ROS↑, mtDam↑,
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↓,
355- AgNPs,    Cytotoxicity and Genotoxicity of Biogenic Silver Nanoparticles in A549 and BEAS-2B Cell Lines
- in-vitro, Lung, A549 - in-vitro, NA, BEAS-2B
ROS↑, DNAdam↑, Apoptosis↑,
357- AgNPs,    Hypoxia-mediated autophagic flux inhibits silver nanoparticle-triggered apoptosis in human lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Lung, L132
mtDam↑, ROS↑, Hif1a↑, LC3s↑, p62↑, eff↓,
231- AL,    Molecular Docking Studies with Garlic Phytochemical Constituents to Inhibit the Human EGFR Protein for Lung Cancer Therapy
- Analysis, Lung, NA
EGFR↓, ROS↑,
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↑,
281- ALA,    Reactive oxygen species mediate caspase activation and apoptosis induced by lipoic acid in human lung epithelial cancer cells through Bcl-2 down-regulation
- in-vitro, Lung, H460
mt-ROS↑, Apoptosis↑, Casp9↑, Bcl-2↓, eff↓, eff↑, H2O2↑, Dose↑,
267- ALA,    α-Lipoic Acid Targeting PDK1/NRF2 Axis Contributes to the Apoptosis Effect of Lung Cancer Cells
- vitro+vivo, Lung, A549 - vitro+vivo, Lung, PC9
Apoptosis↑, ROS↑, PDK1↓, NRF2↓, PDK1↓, Bcl-2↓, Casp9↑, Dose∅,
1349- And,    Andrographolide promoted ferroptosis to repress the development of non-small cell lung cancer through activation of the mitochondrial dysfunction
- in-vitro, Lung, H460 - in-vitro, Lung, H1650
TumCG↓, TumMeta↓, Ferroptosis↑, ROS↑, MDA↑, Iron↑, GSH↓, GPx4↓, xCT↓, MMP↓, ATP↓,
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↓,
206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, lactateProd↓, PGK1↓, ALDOA↓, GLUT1↓, ENO1↓, ATP↓, Casp9↑, Casp3↑, cl‑PARP↑, PI3K/Akt↓, HK1↓, HK2↓, ROS↑, Apoptosis↑, eff↓, NADPH↓, PPP↓,
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↑,
2575- ART/DHA,  docx,    Artemisia santolinifolia-Mediated Chemosensitization via Activation of Distinct Cell Death Modes and Suppression of STAT3/Survivin-Signaling Pathways in NSCLC
- in-vitro, Lung, H23
ChemoSen↑, GPx4↓, ROS↑, Ferroptosis↑, eff↑,
1370- Ash,    Withaferin A induces mitochondrial-dependent apoptosis in non-small cell lung cancer cells via generation of reactive oxygen species
- in-vitro, Lung, A549
ROS↑, eff↓,
1360- Ash,  immuno,    Withaferin A Increases the Effectiveness of Immune Checkpoint Blocker for the Treatment of Non-Small Cell Lung Cancer
- in-vitro, Lung, H1650 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
PD-L1↑, eff↓, ROS↑, ER Stress↑, Apoptosis↑, BAX↑, Bak↑, BAD↑, Bcl-2↓, XIAP↓, survivin↓, cl‑PARP↑, CHOP↑, p‑eIF2α↑, ICD↑, eff↑,
1525- Ba,  almon,    Synergistic antitumor activity of baicalein combined with almonertinib in almonertinib-resistant non-small cell lung cancer cells through the reactive oxygen species-mediated PI3K/Akt pathway
- in-vitro, Lung, H1975 - in-vivo, Lung, NA
eff↑, TumCP↓, Apoptosis↑, cl‑Casp3↑, cl‑PARP↑, cl‑Casp9↑, p‑PI3K↓, p‑Akt↓, ROS↑, eff↓,
1524- Ba,    ROS_and_the_Activation_of_AMPK_in_Human_Lung_Carcinoma_A549_Cells">Baicalein Induces Caspase‐dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
DR5↑, FADD↑, FasL↑, Casp8↑, cFLIP↓, Casp3↑, Casp9↑, cl‑PARP↑, MMP↓, BID↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑, Apoptosis↑, TumCCA↑, DR5↑, FasL↑, DR4∅, cFLIP↓, FADD↑, MMPs↓,
2476- Ba,    Baicalein Induces Caspase-dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
TumCG↓, Apoptosis↑, DR5↑, FasL↑, FADD↑, Casp8↑, cFLIP↓, Casp9↑, Casp3↑, cl‑PARP↑, MMP↓, BID↑, BAX↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑,
1397- BBR,  Chemo,    Effects of Coptis extract combined with chemotherapeutic agents on ROS production, multidrug resistance, and cell growth in A549 human lung cancer cells
- in-vitro, Lung, A549
TumCG↓, ROS↑, MDR1↓,
2699- BBR,    Plant Isoquinoline Alkaloid Berberine Exhibits Chromatin Remodeling by Modulation of Histone Deacetylase To Induce Growth Arrest and Apoptosis in the A549 Cell Line
- in-vitro, Lung, A549
HDAC↓, TumCCA↑, TNF-α↓, COX2↓, MMP2↓, MMP9↓, P21↑, P53↑, Casp↑, ac‑H3↑, ac‑H4↑, ROS↑, MMP↓,
5703- BRU,    Brusatol Enhances the Radiosensitivity of A549 Cells by Promoting ROS Production and Enhancing DNA Damage
- in-vitro, Lung, H1299 - in-vitro, Lung, A549 - in-vitro, Lung, H460
NRF2↓, RadioS↑, DNAdam↑, ROS↑,
1259- CAP,    Capsaicin inhibits HIF-1α accumulation through suppression of mitochondrial respiration in lung cancer cells
- in-vitro, Lung, H1299 - in-vitro, Lung, A549 - in-vitro, Lung, H23 - in-vitro, Lung, H2009
Hif1a↓, PDK1↓, GLUT1↓, ROS↑, mitResp↓, ATP↓,
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↑,
5819- CBD,    The potential role of cannabidiol (CBD) in lung cancer therapy: a systematic review of preclinical and clinical evidence
- Review, Lung, NA
Apoptosis↑, PPARγ↓, mtDam↑, ROS↑, EMT↓, CD8+↑, NK cell↑, ChemoSen↑, ATP↓, glucose↓, Ca+2↑, TRPV2↑,
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↑,
6131- CHr,  Bor,  Z,    Fabrication of phenyl boronic acid modified pH-responsive zinc oxide nanoparticles as targeted delivery of chrysin on human A549 cells
- in-vitro, Lung, A549
*BioAv↑, ROS↑, TumCD↑, TumCCA↑, MMP2↓, TumMeta↓, TumCI↓, GSH↓, eff↑,
2801- CHr,    AMP-activated protein kinase (AMPK) activation is involved in chrysin-induced growth inhibition and apoptosis in cultured A549 lung cancer cells
- in-vitro, Lung, A549
AMPK↑, Akt↓, ChemoSen↑, ROS↑,
1602- Cu,    A simultaneously GSH-depleted bimetallic Cu(ii) complex for enhanced chemodynamic cancer therapy†
- in-vitro, BC, MCF-7 - in-vitro, BC, 4T1 - in-vitro, Lung, A549 - in-vitro, Liver, HepG2
eff↑, GSH↓, H2O2↑, ROS↑, *BioAv↑, selectivity↑, TumCCA↑, Apoptosis↑, Fenton↑, *toxicity?,
2978- CUR,    N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells
- in-vitro, Lung, A549
ROS↑, hTERT/TERT↓, Sp1/3/4↓, eff↓,
1981- CUR,    Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- in-vitro, Lung, NA
eff↑, ROS↑, mt-GSH↓, Bax:Bcl2↑, Cyt‑c↑, MMP↓, Casp3↑, Trx2↓, TrxR↓, mt-DNAdam↑,
1979- CUR,  Rad,    Dimethoxycurcumin, a metabolically stable analogue of curcumin enhances the radiosensitivity of cancer cells: Possible involvement of ROS and thioredoxin reductase
- in-vitro, Lung, A549
eff↑, ROS↑, GSH/GSSG↓, TrxR↓, selectivity↑,
1408- CUR,    Antiproliferative and ROS Regulation Activity of Photoluminescent Curcumin-Derived Nanodots
- in-vitro, Lung, A549
ROS↓, ROS↑,
1608- EA,    Ellagic Acid from Hull Blackberries: Extraction, Purification, and Potential Anticancer Activity
- in-vitro, Cerv, HeLa - in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, HUVECs
eff↑, Dose∅, *BioAv↑, selectivity↑, TumCP↓, Casp↑, PTEN↑, TSC1↑, mTOR⇅, Akt↓, PDK1↓, E6↓, E7↓, DNAdam↑, ROS↑, *BioAv↓, *BioEnh↑, *Half-Life∅,
3219- EGCG,    Nano-chemotherapeutic efficacy of (−) -epigallocatechin 3-gallate mediating apoptosis in A549 cells: Involvement of reactive oxygen species mediated Nrf2/Keap1signaling
- in-vitro, Lung, A549
ROS↑, RNS↓, MMP↓, NRF2↑, Keap1↓,
1327- EMD,    Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway
- in-vitro, Lung, A549
Cyt‑c↑, Casp2↑, Casp3↑, Casp9↑, ERK↓, Akt↓, ROS↑, MMP↓, Bcl-2↓, BAX↑,
1326- EMD,    Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cells
- in-vitro, Lung, A549
Apoptosis↑, ROS↑, P53↑, BAX↑, ATM↑,
1963- GamB,    Gambogic acid exhibits promising anticancer activity by inhibiting the pentose phosphate pathway in lung cancer mouse model
- in-vitro, Lung, NA
ROS↑, 6PGD↓, PPP↓,
1966- GamB,  Cisplatin,    Gambogic acid synergistically potentiates cisplatin-induced apoptosis in non-small-cell lung cancer through suppressing NF-κB and MAPK/HO-1 signalling
- in-vitro, Lung, A549 - in-vitro, Lung, NCIH1299
TumCCA↑, PARP↑, eff↑, ROS↑, ChemoSen↑,
1968- GamB,    Gambogic Acid Shows Anti-Proliferative Effects on Non-Small Cell Lung Cancer (NSCLC) Cells by Activating Reactive Oxygen Species (ROS)-Induced Endoplasmic Reticulum (ER) Stress-Mediated Apoptosis
- in-vitro, Lung, A549
tumCV↓, ROS↑, GRP78/BiP↑, CHOP↑, ATF6↑, Casp12↑, p‑PERK↑, ER Stress↑,
1970- GamB,    Gambogic acid-induced autophagy in nonsmall cell lung cancer NCI-H441 cells through a reactive oxygen species pathway
- NA, Lung, NCI-H441
TumCG↓, TumAuto↑, Beclin-1↑, LC3‑Ⅱ/LC3‑Ⅰ↑, ROS↑, eff↓,

Showing Research Papers: 1 to 50 of 105
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 105

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   Fenton↑, 1,   Ferroptosis↑, 2,   GPx4↓, 2,   GSH↓, 5,   mt-GSH↓, 1,   GSH/GSSG↓, 1,   GSSG↑, 1,   H2O2↑, 2,   HK1↓, 1,   HO-1↑, 1,   ICD↑, 1,   Iron↑, 1,   Keap1↓, 1,   MDA↑, 2,   NRF2↓, 2,   NRF2↑, 1,   OXPHOS↑, 1,   RNS↓, 1,   ROS↓, 1,   ROS↑, 48,   mt-ROS↑, 2,   selenoP↓, 1,   SOD2↑, 1,   Thiols↓, 1,   Trx2↓, 1,   TrxR↓, 5,   TrxR1↓, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 6,   mitResp↓, 1,   MMP↓, 10,   mtDam↑, 5,   OCR↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

6PGD↓, 1,   ALDOA↓, 1,   AMPK↑, 3,   ENO1↓, 1,   glucose↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 2,   LDH↓, 1,   LDH↑, 1,   NADPH↓, 1,   PDK1↓, 4,   PGK1↓, 1,   PI3K/Akt↓, 1,   PPARγ↓, 1,   PPP↓, 2,   p‑S6↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 1,   Apoptosis↑, 19,   BAD↑, 1,   Bak↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   BID↑, 2,   Casp↑, 3,   Casp12↑, 1,   Casp2↑, 1,   Casp3↑, 10,   cl‑Casp3↑, 1,   Casp8↑, 3,   Casp9↑, 10,   cl‑Casp9↑, 1,   cFLIP↓, 3,   Cyt‑c↑, 7,   DR4∅, 1,   DR5↑, 3,   FADD↑, 3,   FasL↑, 3,   Ferroptosis↑, 2,   hTERT/TERT↓, 1,   p‑JNK↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,   TRPV2↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   tumCV↓, 4,   tumCV↑, 1,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   CHOP↓, 1,   CHOP↑, 2,   p‑eIF2α↓, 1,   p‑eIF2α↑, 1,   ER Stress↑, 4,   GRP78/BiP↓, 1,   GRP78/BiP↑, 1,   IRE1↑, 1,   p‑PERK↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3s↑, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 5,   mt-DNAdam↑, 1,   P53↓, 1,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 5,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 9,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   EMT↓, 1,   ERK↓, 1,   HDAC↓, 1,   mTOR↓, 2,   mTOR⇅, 1,   PI3K↓, 1,   p‑PI3K↓, 1,   PTEN↑, 1,   TumCG↓, 4,  

Migration ⓘ

Ca+2↑, 2,   MMP2↓, 3,   MMP9↓, 2,   MMPs↓, 1,   TSC1↑, 1,   TumCI↓, 4,   TumCMig↓, 4,   TumCP↓, 5,   TumMeta↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   EPR↑, 1,   Hif1a↓, 1,   Hif1a↑, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

CTR1↑, 1,   GLUT1↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   p‑NF-kB↑, 1,   NK cell↑, 1,   PD-L1↑, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 5,   Dose↑, 1,   Dose↝, 2,   Dose∅, 2,   eff↓, 12,   eff↑, 14,   eff↝, 2,   MDR1↓, 1,   RadioS↑, 2,   selectivity↑, 6,  

Clinical Biomarkers ⓘ

E6↓, 1,   E7↓, 1,   EGFR↓, 1,   hTERT/TERT↓, 1,   LDH↓, 1,   LDH↑, 1,   PD-L1↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 2,   toxicity↓, 1,   TumW↓, 1,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 171

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 3,   BioEnh↑, 1,   Half-Life∅, 1,  

Functional Outcomes ⓘ

toxicity?, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 7

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
13 Silver-NanoParticles
8 Radiotherapy/Radiation
7 Magnetic Fields
6 Piperlongumine
5 Curcumin
4 Gambogic Acid
4 Lycopene
4 Resveratrol
4 Magnetic Field Rotating
4 Shikonin
4 Selenite (Sodium)
3 Baicalein
3 Berberine
2 Allicin (mainly Garlic)
2 Alpha-Lipoic-Acid
2 Apigenin (mainly Parsley)
2 Artemisinin
2 Ashwagandha(Withaferin A)
2 Chemotherapy
2 chitosan
2 Chrysin
2 Emodin
2 Gold NanoParticles
2 Honokiol
2 Vitamin C (Ascorbic Acid)
2 Quercetin
2 Propyl gallate
2 Sulforaphane (mainly Broccoli)
1 5-Aminolevulinic acid
1 Auranofin
1 entinostat
1 Andrographis
1 2-DeoxyGlucose
1 Docetaxel
1 immunotherapy
1 almonertinib
1 brusatol
1 Capsaicin
1 Carvacrol
1 Cannabidiol
1 Boron
1 Zinc
1 Copper and Cu NanoParticles
1 Ellagic acid
1 EGCG (Epigallocatechin Gallate)
1 Cisplatin
1 Graviola
1 Hydroxycinnamic-acid
1 Juglone
1 Luteolin
1 Methylene blue
1 Photodynamic Therapy
1 Magnolol
1 Melatonin
1 Metformin
1 Myricetin
1 Naringin
1 Phenylbutyrate
1 Phenethyl isothiocyanate
1 Sanguinarine
1 Rosmarinic acid
1 SonoDynamic Therapy UltraSound
1 Selenium
1 Selenium NanoParticles
1 Osimertinib
1 Adagrasib
1 Thymoquinone
1 VitK3,menadione
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:15  Cells:%  prod#:%  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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