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


CRC, Colorectal Cancer: Click to Expand ⟱
Colorectal cancer is a broader term that encompasses both colon and rectal cancer.
Scientific Papers found: Click to Expand⟱
5263- 3BP,  CET,    3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis
- in-vitro, CRC, DLD1 - NA, NA, HCT116
eff↑, Ferroptosis↓, TumAuto↑, Apoptosis↑, FOXO3↑, AMPKα↑, p‑Beclin-1↑, HK2↓, ATP↓, ROS↑, Dose↝, TumVol↓, TumW↓, xCT↑, GSH↓, eff↓, MDA↑,
4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, TumCCA↑, Apoptosis↑, eff↑, Bcl-2↓, survivin↓, P21↑, p27↑, BAX↑, Cyt‑c↑, Casp3↑, PI3K↓, Akt↓, mTOR↓, Hif1a↓, PTEN↑, AMPKα↑, PDH↑, LDHA↓, antiOx↓, ROS↑, AntiCan↑,
4403- AgNPs,    Silver Nanoparticles Decorated UiO-66-NH2 Metal-Organic Framework for Combination Therapy in Cancer Treatment
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vitro, GBM, GL26 - in-vitro, Cerv, HeLa - in-vitro, CRC, RKO
AntiCan↑, eff↑, EPR↑, selectivity↑, ROS↑, Casp↑, Apoptosis↑, DNAdam↑, tumCV↓, eff↑,
4362- AgNPs,    Enhancing Colorectal Cancer Radiation Therapy Efficacy using Silver Nanoprisms Decorated with Graphene as Radiosensitizers
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vivo, NA, NA
eff↑, TumCG↓, OS↑, RadioS↑, eff↑, ROS↑, DNAdam↑, eff↝,
4379- AgNPs,    Exposure to silver nanoparticles induces size- and dose-dependent oxidative stress and cytotoxicity in human colon carcinoma cells
- in-vitro, CRC, LoVo
eff↑, TumCD↑, ROS↑, Bacteria↓,
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↑,
4559- AgNPs,    Anticancer activity of biogenerated silver nanoparticles: an integrated proteomic investigation
- in-vitro, BC, SkBr3 - in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, Colon, Caco-2
MMP2↓, MMP9↓, ROS↑, TumAuto↑, Apoptosis↑, ER Stress↑,
4557- AgNPs,    The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells
- in-vitro, NA, NIH-3T3 - in-vitro, CRC, HCT116
Cyt‑c↑, ROS↑, JNK↑,
5143- AgNPs,    Thermal Co-reduction engineered silver nanoparticles induce oxidative cell damage in human colon cancer cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis
- in-vitro, CRC, HCT116
ROS↑, lipid-P↑, GSH↓, MMP↓, Casp3↑, Apoptosis↑, TumCCA↑,
5142- AgNPs,    Biosynthesized Protein-Capped Silver Nanoparticles Induce ROS-Dependent Proapoptotic Signals and Prosurvival Autophagy in Cancer Cells
- in-vitro, CRC, HUH7
ROS↑, Apoptosis↑, eff↑, ChemoSen↑, EPR↑, Casp↑, MAPK↑,
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↑,
1351- And,  MEL,    Impact of Andrographolide and Melatonin Combinatorial Drug Therapy on Metastatic Colon Cancer Cells and Organoids
- in-vitro, CRC, T84 - in-vitro, CRC, COLO205 - in-vitro, CRC, HT-29 - in-vitro, CRC, DLD1
eff↑, Ki-67↓, Casp3↑, ER Stress↑, ROS↑, BAX↑, XBP-1↑, CHOP↑, eff↑,
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↑,
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↓,
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↑,
2582- ART/DHA,  5-ALA,    Mechanistic Investigation of the Specific Anticancer Property of Artemisinin and Its Combination with Aminolevulinic Acid for Enhanced Anticolorectal Cancer Activity
- in-vivo, CRC, HCT116 - in-vitro, CRC, HCT116
eff↑, ROS↑, selectivity↑, TumCG↓, toxicity↓,
1356- Ash,    Withaferin A induces apoptosis by ROS-dependent mitochondrial dysfunction in human colorectal cancer cells
- in-vitro, CRC, HCT116
ROS↑, TumCCA↑, MMP↓, TumCG↓, Apoptosis↑, JNK↝,
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↑,
1375- BBR,    13-[CH2CO-Cys-(Bzl)-OBzl]-Berberine: Exploring The Correlation Of Anti-Tumor Efficacy With ROS And Apoptosis Protein
- in-vitro, CRC, HCT8 - in-vivo, NA, NA
ROS↑, TumCP↓, XIAP↓, TumCG↓, *toxicity↓,
2734- BetA,    Betulinic Acid Modulates the Expression of HSPA and Activates Apoptosis in Two Cell Lines of Human Colorectal Cancer
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW480
tumCV↓, HSP70/HSPA5⇅, ROS↑, cl‑Casp3↑, mt-Apoptosis↑, Dose↝,
2745- BetA,    Betulinic acid inhibits colon cancer cell and tumor growth and induces proteasome-dependent and -independent downregulation of specificity proteins (Sp) transcription factors
- in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vivo, NA, NA
Apoptosis↑, TumCG↓, Sp1/3/4↓, survivin↓, VEGF↓, p65↓, EGFR↓, cycD1/CCND1↓, ROS↑, MMP↓,
2746- BetA,    Betulinic acid induces apoptosis and inhibits metastasis of human colorectal cancer cells in vitro and in vivo
- in-vitro, CRC, HCT116 - in-vivo, CRC, NA
TumCG↓, BAX↑, Bcl-2↓, ROS↑, MMP↓, TIMP2↑, TumVol↓,
5678- BML,    Bromelain inhibits the ability of colorectal cancer cells to proliferate via activation of ROS production and autophagy
- in-vivo, CRC, NA
AntiCan↑, TumCG↓, ROS↑, Apoptosis↑, Endoglin↑, Casp3↑, Casp8↑, Casp9↑, ATG5↑, Beclin-1↑, p62↑, PARP↑,
5707- Brut,    Targeting Redox Homeostasis and Cell Survival Signaling with a Flavonoid-Rich Extract of Bergamot Juice in In Vitro and In Vivo Colorectal Cancer Models
- in-vitro, CRC, HCT116
Risk↓, TumCG↓, Apoptosis↑, TumCCA↑, ROS↑, MMP↓, DNAdam↑, TumMeta↓, TumCP↓,
5706- Brut,    Bergamot juice extract inhibits proliferation by inducing apoptosis in human colon cancer cells
- in-vitro, CRC, HT29
TumCG↓, MAPK↓, TumCCA↑, Apoptosis↑, ROS↑, DNAdam↑, AntiCan↑,
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↓,
5877- CA,    Carnosol induces apoptosis through generation of ROS and inactivation of STAT3 signaling in human colon cancer HCT116 cells
- in-vitro, CRC, HCT116
tumCV↓, Apoptosis↑, Casp9↑, Casp3↑, cl‑PARP↑, BAX↑, Bcl-2↓, Bcl-xL↓, P53↓, MDM2↓, ROS↑, eff↓, STAT3↓, survivin↓, cycD1/CCND1↓,
5866- CA,    Carnosic acid inhibits STAT3 signaling and induces apoptosis through generation of ROS in human colon cancer HCT116 cells
- in-vitro, CRC, HCT116 - in-vitro, Colon, SW480 - in-vitro, Colon, HT29
tumCV↓, Apoptosis↑, P53↑, BAX↑, MDM2↓, Bcl-2↓, Bcl-xL↓, Casp9↑, Casp3↑, cl‑PARP↑, STAT3↓, survivin↓, cycD1/CCND1↓, CycD3↓, ROS↑, eff↓, eff↑,
5198- CAP,    Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines
- in-vitro, CRC, LoVo - in-vitro, CRC, Colo320
tumCV↓, DNAdam↑, Apoptosis↑, ROS↑, MMP↑, Casp3↑, chemoPv↑,
1517- CAP,    Capsaicin Inhibits Multiple Bladder Cancer Cell Phenotypes by Inhibiting Tumor-Associated NADH Oxidase (tNOX) and Sirtuin1 (SIRT1)
- in-vitro, Bladder, TSGH8301 - in-vitro, CRC, T24/HTB-9
ENOX2↓, TumCCA↑, ERK↓, p‑FAK↓, p‑pax↓, TumCMig↓, EMT↓, SIRT1↓, Dose∅, ROS↑, MMP↓, Bcl-2↓, Bak↑, cl‑PARP↑, Casp3↑, SIRT1↓, ac‑P53↑, BIM↑, p‑RB1↓, cycD1/CCND1↓, Dose∅, β-catenin/ZEB1↓, N-cadherin↓, E-cadherin↑,
2804- CHr,  Rad,    Gamma-Irradiated Chrysin Improves Anticancer Activity in HT-29 Colon Cancer Cells Through Mitochondria-Related Pathway
- in-vitro, CRC, HT29
RadioS↑, ROS↑, MMP↓, Casp3↑, Casp9↑, cl‑PARP↑,
1601- Cu,    The copper (II) complex of salicylate phenanthroline induces immunogenic cell death of colorectal cancer cells through inducing endoplasmic reticulum stress
- in-vitro, CRC, NA
i-CRT↓, ICD↑, i-ATP↓, i-HMGB1↓, ER Stress↑, ROS↑, DCells↑, CD8+↑, IL12↑, IFN-γ↑, TGF-β↓,
405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, TumCMig↓, NRF2↑, ROS↑, MET↑, miR-34a↑,
448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑, TumCCA↑, p‑Akt↓, Akt↓, Bcl-2↓, p‑BAD↓, BAD↑, cl‑PARP↑, ROS↑, HSP27↑, Beclin-1↑, p62↑, GPx1↓, GPx4↓,
440- CUR,    Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, HT-29
NNMT↓, p‑STAT3↓, TumCP↓, TumCCA↑, ROS↑,
1869- DCA,    Dichloroacetate induces autophagy in colorectal cancer cells and tumours
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29
LC3II↑, ROS↑, mTOR↓, MCT1↓, NADH:NAD↓, NAD↑, TumAuto↑, lactateProd↓, LDH↑,
1885- DCA,    Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW-620 - in-vitro, CRC, HT-29
SMCT1∅, eff↓, eff↑, eff↑, PDKs↓, MMP↓, Glycolysis↓, mitResp↑, ROS↑, eff↑,
3214- EGCG,    EGCG-induced selective death of cancer cells through autophagy-dependent regulation of the p62-mediated antioxidant survival pathway
- in-vitro, Nor, MRC-5 - in-vitro, Cerv, HeLa - in-vitro, Nor, HEK293 - in-vitro, BC, MDA-MB-231 - in-vitro, CRC, HCT116
mTOR↓, AMPK↑, selectivity↑, ROS↑, selectivity↑, HO-1↓, *NRF2↑, NRF2↓, *HO-1↑,
1321- EMD,    Antitumor effects of emodin on LS1034 human colon cancer cells in vitro and in vivo: roles of apoptotic cell death and LS1034 tumor xenografts model
- in-vitro, CRC, LS1034 - in-vivo, NA, NA
tumCV↓, TumCCA↑, ROS↑, Ca+2↑, MMP↓, Apoptosis↑, Cyt‑c↑, Casp9↑, Bax:Bcl2↑,
2852- FIS,    A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms
- Review, CRC, NA
Risk↓, P53↑, MDM2↓, COX2↓, Wnt↓, NF-kB↓, CDK2↓, CDK4↓, p‑RB1↓, cycE/CCNE↓, P21↑, NRF2↓, ROS↑, Casp8↑, Fas↑, TRAIL↑, DR5↑, MMP↓, Cyt‑c↑, selectivity↑, P450↝, GSTs↝, RadioS↑, Inflam↓, β-catenin/ZEB1↓, EGFR↓, TumCCA↑, ChemoSen↑,
823- GAR,    Garcinol Potentiates TRAIL-Induced Apoptosis through Modulation of Death Receptors and Antiapoptotic Proteins
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10 - in-vitro, CRC, HCT116
Casp3↑, Casp9↑, Casp8↑, DR5↑, survivin↓, Bcl-2↓, XIAP↓, cFLIP↓, BAX↑, Cyt‑c↑, ROS↑, GSH↓, *eff↓,
858- Gra,    Annona muricata leaves induce G₁ cell cycle arrest and apoptosis through mitochondria-mediated pathway in human HCT-116 and HT-29 colon cancer cells
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116
TumCCA↑, Apoptosis↑, ROS↑, MMP↓, Cyt‑c↑, Casp↑, BAX↑, Bcl-2↓, TumCMig↓, TumCI↓,
848- Gra,  AgNPs,    Synthesis, Characterization and Evaluation of Antioxidant and Cytotoxic Potential of Annona muricata Root Extract-derived Biogenic Silver Nanoparticles
- in-vitro, CRC, HCT116
ROS↑, PUMA↝, Casp3↑, Casp8↑, Casp9↑, Apoptosis↑,
4638- HT,    Hydroxytyrosol induces apoptosis in human colon cancer cells through ROS generation
- in-vitro, CRC, DLD1 - NA, NA, 1-
selectivity↑, ROS↑, Akt↑, FOXO3↓, Apoptosis↑,
4641- HT,    Hydroxytyrosol induced ferroptosis through Nrf2 signaling pathway in colorectal cancer cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW48
Ferroptosis↑, Iron↑, lipid-P↑, ROS↑, GSH↓, MMP↓, GPx4↓, TLR1↑, eff↓, NRF2↓, ROS↑,
2534- M-Blu,  doxoR,  PDT,    Methylene Blue-Mediated Photodynamic Therapy in Combination With Doxorubicin: A Novel Approach in the Treatment of HT-29 Colon Cancer Cells
- in-vitro, CRC, HT-29
LDH↑, ROS↑,
2251- MF,  Rad,    BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage
- in-vitro, Lung, A549 - in-vitro, HNSCC, UTSCC15 - in-vitro, CRC, DLD1 - in-vitro, PC, MIA PaCa-2
RadioS↑, DNAdam↑, ROS↑, ChemoSen∅, Pyruv↓, ADP:ATP↓, ROS↑,
5215- PI,    Piperine impairs cell cycle progression and causes reactive oxygen species-dependent apoptosis in rectal cancer cells
- in-vitro, CRC, NA
TumCCA↑, Apoptosis↑, ROS↑, eff↓, BioEnh↑,
5214- PI,    Piperine induces autophagy of colon cancer cells: Dual modulation of AKT/mTOR signaling pathway and ROS production
- vitro+vivo, CRC, HCT116 - in-vitro, CRC, SW48 - in-vitro, CRC, SW-620
TumCP↓, TumAuto↑, Akt↓, mTOR↓, ROS↑,
1949- PL,    Design, synthesis, and biological evaluation of a novel indoleamine 2,3-dioxigenase 1 (IDO1) and thioredoxin reductase (TrxR) dual inhibitor
- in-vitro, CRC, HCT116 - in-vitro, Cerv, HeLa
TrxR↓, selectivity↑, ROS↑, IDO1↓,

Showing Research Papers: 1 to 50 of 78
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 78

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   ENOX2↓, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 2,   GPx1↓, 1,   GPx4↓, 2,   GSH↓, 5,   GSSG↑, 1,   GSTs↝, 1,   HK1↓, 1,   HO-1↓, 1,   ICD↑, 2,   Iron↑, 2,   lipid-P↑, 3,   MDA↑, 1,   NRF2↓, 3,   NRF2↑, 2,   PARK2↑, 1,   ROS↑, 52,   Thiols↓, 1,   TrxR↓, 1,   xCT↑, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↓, 1,   ATP↓, 2,   i-ATP↓, 1,   ETC↓, 1,   mitResp↑, 1,   MMP↓, 15,   MMP↑, 1,   mtDam↑, 1,   PINK1↑, 1,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   AMPK↑, 2,   ENO1↓, 1,   Glycolysis↓, 2,   HK2↓, 2,   IDO1↓, 1,   lactateProd↓, 2,   LDH↑, 2,   LDHA↓, 1,   NAD↑, 1,   NADH:NAD↓, 1,   NADPH↓, 1,   NNMT↓, 1,   PDH↑, 1,   PDKs↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 1,   PPP↓, 1,   Pyruv↓, 1,   SIRT1↓, 2,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 25,   mt-Apoptosis↑, 1,   BAD↑, 2,   p‑BAD↓, 1,   Bak↑, 2,   BAX↑, 10,   Bax:Bcl2↑, 1,   Bcl-2↓, 10,   Bcl-xL↓, 3,   cl‑BID↑, 1,   BIM↑, 1,   Casp↑, 3,   Casp3↑, 12,   cl‑Casp3↑, 3,   Casp8↑, 4,   cl‑Casp8↑, 1,   Casp9↑, 8,   cl‑Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 7,   DR5↑, 3,   Fas↑, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 2,   JNK↑, 1,   JNK↝, 1,   MAPK↓, 1,   MAPK↑, 1,   MCT1↓, 1,   MDM2↓, 3,   p27↑, 1,   PUMA↝, 1,   survivin↓, 6,   TRAIL↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 2,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 7,  

Protein Folding & ER Stress ⓘ

CHOP↑, 3,   i-CRT↓, 1,   p‑eIF2α↑, 1,   ER Stress↑, 5,   HSP27↑, 1,   HSP70/HSPA5⇅, 1,   UPR↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 2,   p‑Beclin-1↑, 1,   LC3II↑, 3,   p62↓, 1,   p62↑, 2,   TumAuto↑, 6,  

DNA Damage & Repair ⓘ

DNAdam↑, 7,   P53↓, 1,   P53↑, 2,   ac‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 8,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 4,   CycD3↓, 1,   cycE/CCNE↓, 1,   P21↑, 2,   p‑RB1↓, 2,   TumCCA↑, 14,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   EMT↓, 1,   ERK↓, 1,   FOXO3↓, 1,   FOXO3↑, 1,   HDAC↓, 1,   miR-34a↑, 1,   mTOR↓, 4,   mTOR↑, 1,   PI3K↓, 1,   PTEN↑, 1,   STAT3↓, 2,   p‑STAT3↓, 1,   TumCG↓, 11,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 2,   p‑FAK↓, 1,   Ki-67↓, 1,   MET↑, 1,   miR-139-5p↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 2,   p‑pax↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TumCI?, 1,   TumCI↓, 1,   TumCMig↓, 4,   TumCP↓, 5,   TumMeta↓, 2,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 2,   Endoglin↑, 1,   EPR↑, 2,   Hif1a↓, 2,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   SMCT1∅, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   DCells↑, 1,   i-HMGB1↓, 1,   IFN-γ↑, 1,   IL12↑, 1,   Inflam↓, 1,   NF-kB↓, 1,   p65↓, 1,   PD-L1↑, 1,   TLR1↑, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   ChemoSen↑, 2,   ChemoSen∅, 1,   Dose↝, 2,   Dose∅, 2,   eff↓, 9,   eff↑, 18,   eff↝, 1,   P450↝, 1,   RadioS↑, 4,   selectivity↑, 8,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   Ferritin↓, 1,   Ki-67↓, 1,   LDH↑, 2,   PD-L1↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 6,   AntiTum↑, 1,   chemoPv↑, 1,   OS↑, 1,   Risk↓, 2,   toxicity↓, 1,   TumVol↓, 2,   TumW↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   CD8+↑, 1,  
Total Targets: 202

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NRF2↑, 1,  

Cell Death ⓘ

JNK↑, 1,  

Protein Folding & ER Stress ⓘ

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

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,   toxicity↝, 1,  

Infection & Microbiome ⓘ

AntiViral↑, 1,  
Total Targets: 11

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
9 Silver-NanoParticles
6 Shikonin
5 Piperlongumine
5 Selenite (Sodium)
3 5-fluorouracil
3 Thymoquinone
3 Betulinic acid
3 Curcumin
2 Vitamin C (Ascorbic Acid)
2 Apigenin (mainly Parsley)
2 Artemisinin
2 Ashwagandha(Withaferin A)
2 Bruteridin(bergamot juice)
2 Carnosic acid
2 Capsaicin
2 Radiotherapy/Radiation
2 Dichloroacetate
2 Graviola
2 HydroxyTyrosol
2 Piperine
2 salinomycin
2 Cisplatin
2 Sulforaphane (mainly Broccoli)
1 3-bromopyruvate
1 cetuximab
1 Coenzyme Q10
1 Allicin (mainly Garlic)
1 Andrographis
1 Melatonin
1 5-Aminolevulinic acid
1 immunotherapy
1 Berberine
1 Bromelain
1 Butyrate
1 Chrysin
1 Copper and Cu NanoParticles
1 EGCG (Epigallocatechin Gallate)
1 Emodin
1 Fisetin
1 Garcinol
1 Methylene blue
1 doxorubicin
1 Photodynamic Therapy
1 Magnetic Fields
1 Parthenolide
1 Quercetin
1 Oxaliplatin
1 Sulfasalazine
1 Scoulerine
1 Ursolic acid
1 Urolithin
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:6  Cells:%  prod#:%  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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