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
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Var, Various Cancer: Click to Expand ⟱

Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.

Scientific Papers found: Click to Expand⟱

5355-

AL,

Mini-review: The health benefits and applications of allicin

Review,

Var,

*BioAv↑, *cardioP↑, *hepatoP↑, *RenoP↑, *Half-Life↝, *BioAv↓, *neuroP↑, *cognitive↑, *ROS↓, *lipid-P↓, *DNArepair↑, *ChemoSen↑,

2660-

AL,

Allicin: A review of its important pharmacological activities

Review,

AD,

Review,

Var,

Review,

Park,

Review,

Stroke,

*Inflam↓, AntiCan↑, *antiOx↑, *cardioP↑, *hepatoP↑, *BBB↑, *Half-Life↝, *H2S↑, *BP↓, *neuroP↑, *cognitive↑, *neuroP↑, *ROS↓, *GutMicro↑, *LDH↓, *ROS↓, *lipid-P↓, *antiOx↑, *other↑, *PI3K↓, *Akt↓, *NF-kB↓, *NO↓, *iNOS↓, *PGE2↓, *COX2↓, *IL6↓, *TNF-α↓, *MPO↓, *eff↑, *NRF2↑, *Keap1↓, *TBARS↓, *creat↓, *LDH↓, *AST↓, *ALAT↓, *MDA↓, *SOD↑, *GSH↑, *GSTs↑, *memory↑, chemoP↑, IL8↓, Cyt‑c↑, Casp3↑, Casp8↑, Casp9↑, Casp12↑, p38↑, Fas↑, P53↑, P21↑, CHK1↓, CycB/CCNB1↓, GSH↓, ROS↑, TumCCA↑, Hif1a↓, Bcl-2↓, VEGF↓, TumCMig↓, STAT3↓, VEGFR2↓, p‑FAK↓,

3437-

ALA,

Revisiting the molecular mechanisms of Alpha Lipoic Acid (ALA) actions on metabolism

Review,

Var,

*IronCh↑, *antiOx↑, *ROS↓, *GSH↑, *NF-kB↓, *AMPK⇅, *FAO↑, *GlucoseCon↑, *PI3K↑, *Akt?,

3443-

ALA,

Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention

Review,

Var,

Review,

AD,

*antiOx↑, *ROS↓, *IronCh↑, *cognitive↑, *cardioP↓, AntiCan↑, *neuroP↑, *Inflam↓, *BioAv↓, *AntiAge↑, *Half-Life↓, *BioAv↝, other↝, EGFR↓, Akt↓, ROS↓, TumCCA↑, p27↑, PDH↑, Glycolysis↓, ROS↑, *eff↑, *memory↑, *motorD↑, *GutMicro↑,

3541-

ALA,

Insights on alpha lipoic and dihydrolipoic acids as promising scavengers of oxidative stress and possible chelators in mercury toxicology

Review,

Var,

*antiOx↑, *IronCh↑, *GSH↑, *BBB↑, Apoptosis↑, MMP↓, ROS↑, lipid-P↑, PARP1↑, Casp3↑, Casp9↑, *NRF2↑, *GSH↑, *ROS↓, RenoP↑, ChemoSen↑, *BG↓,

2583-

Api,

Rad,

The influence of apigenin on cellular responses to radiation: From protection to sensitization

Review,

Var,

radioP↑, RadioS↑, *COX2↓, *ROS↓, VEGF↓, MMP2↓, STAT3↓, AMPK↑, Apoptosis↑, MMP9↓, glucose↓,

5396-

Ash,

Withania Somnifera (Ashwagandha) and Withaferin A: Potential in Integrative Oncology

Review,

Var,

selectivity↑, ROS↑, Apoptosis↑, ChemoSen↑, RadioS↑, NF-kB↓, ER-α36↓, P53↑, *ROS∅, γH2AX↑, DNAdam↑, MMP↓, XIAP↓, IAP1↓, survivin↓, SOD↓, Dose↝, IL6↓, TNF-α↓, COX2↓, p‑Akt↓, NOTCH1↓, FOXO↑, Casp↑, MMP2↓, CSCs↓, *ROS↓, *SOD2↑, chemoP↑, ChemoSen↑, RadioS↑,

3166-

Ash,

Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its Derivatives

Review,

Var,

*p‑PPARγ↓, *cardioP↑, *AMPK↑, *BioAv↝, *Half-Life↝, *Half-Life↝, *Dose↑, *chemoPv↑, IL6↓, STAT3↓, ROS↓, OXPHOS↓, PCNA↓, LDH↓, AMPK↑, TumCCA↑, NOTCH3↓, Akt↓, Bcl-2↓, Casp3↑, Apoptosis↑, eff↑, NF-kB↓, CSCs↓, HSP90↓, PI3K↓, FOXO3↑, β-catenin/ZEB1↓, N-cadherin↓, EMT↓, FASN↓, ACLY↓, ROS↑, NRF2↑, HO-1↑, NQO1↑, JNK↑, mTOR↓, neuroP↑, *TNF-α↓, *IL1β↓, *IL6↓, *IL8↓, *IL18↓, RadioS↑, eff↑,

4814-

ASTX,

Chemopreventive and therapeutic efficacy of astaxanthin against cancer: A comprehensive review

Review,

Var,

Apoptosis↑, EMT↓, AntiCan↑, *cardioP↑, *neuroP↑, TumCG↓, *antiOx↑, *Bacteria↓, *Imm↑, *hepatoP↑, *AntiDiabetic↑, ROS↓, *chemoPv↑,

5502-

Ba,

An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways

Review,

Var,

*AntiCan↑, *antiOx↑, *hepatoP↑, *neuroP↑, *ROS↓, Ca+2↑, ROS↑, BAX↑, Casp3↑, Casp9↑, Cyt‑c↑, MMP↓, Mcl-1↓, PI3K↓, Akt↓, mTOR↓, BAD↓, ERK↓, MEK↓, DR5↑, Fas↑, TumMeta↓, EMT↓, SMAD4↓, TGF-β↓, MMP9↓, MMP2↓, HIF-1↓, 12LOX↓,

5251-

Ba,

The Fascinating Effects of Baicalein on Cancer: A Review

Review,

Var,

AntiTum↑, TumCCA↓, ROS↓, MAPK↓, Akt↓, mTOR↓, Casp3↑, Casp9↑, TumCI↓, TumMeta↓, MMP2↓, MMP9↓, Securin↓, γH2AX↝, N-cadherin↓, Vim↓, Zeb1↓, ZEB2↓, TumCMig↓, TumCG↑, 12LOX↓, DR5↑, ROS↑, RadioS↑, ChemoSen↑, BioAv↓,

2474-

Ba,

Anticancer properties of baicalein: a review

Review,

Var,

in-vitro,

Nor,

BV2

ROS⇅, ROS↑, ER Stress↑, Ca+2↑, Apoptosis↑, eff↑, DR5↑, 12LOX↓, Cyt‑c↑, Casp7↑, Casp9↑, Casp3↑, cl‑PARP↑, TumCCA↑, cycE/CCNE↑, CDK4↓, cycD1/CCND1↓, VEGF↓, cMyc↓, Hif1a↓, NF-kB↓, BioEnh↑, BioEnh↑, P450↓, *Hif1a↓, *iNOS↓, *COX2↓, *VEGF↓, *ROS↓, *PI3K↓, *Akt↓,

2605-

Ba,

BA,

Potential therapeutic effects of baicalin and baicalein

Review,

Var,

Review,

Stroke,

Review,

IBD,

Review,

Arthritis,

Review,

AD,

Review,

Park,

cardioP↑, Inflam↓, cognitive↑, *hepatoP↑, *ROS?, *SOD↑, *GSH↑, *MMP↑, *GutMicro↑, ChemoSen↑, *TNF-α↓, *IL10↑, *IL6↓, *eff↑, *ROS↓, *COX2↓, *NF-kB↓, *STAT3↓, *PGE2↓, *MPO↓, *IL1β↓, *MMP2↓, *MMP9↓, *β-Amyloid↓, *neuroP↑, *Dose↝, *BioAv↝, *BioAv↝, *BBB↑, *BDNF↑,

2292-

Ba,

BA,

Baicalin and baicalein in modulating tumor microenvironment for cancer treatment: A comprehensive review with future perspectives

Review,

Var,

AntiCan↑, *toxicity↓, BioAv↝, BioAv↓, *ROS↓, *TLR2↓, *NF-kB↓, *NRF2↑, *antiOx↑, *Inflam↓, HDAC1↓, HDAC8↓, Wnt↓, β-catenin/ZEB1↓, PD-L1↓, Sepsis↓, NF-kB↓, LOX1↓, COX2↓, VEGF↑, PI3K↓, Akt↓, mTOR↓, MMP2↓, MMP9↓, SIRT1↑, AMPK↑,

2674-

BBR,

Berberine: A novel therapeutic strategy for cancer

Review,

Var,

Review,

IBD,

Inflam↓, AntiCan↑, Apoptosis↑, TumAuto↑, TumCCA↑, TumMeta↓, TumCI↓, eff↑, eff↑, CD4+↓, TNF-α↓, IL1↓, BioAv↓, BioAv↓, other↓, AMPK↑, MAPK↓, NF-kB↓, IL6↓, MCP1↓, PGE2↓, COX2↓, *ROS↓, *antiOx↑, *GPx↑, *Catalase↑, AntiTum↑, TumCP↓, angioG↓, Fas↑, FasL↑, ROS↑, ATM↑, P53↑, RB1↑, Casp9↑, Casp8↑, Casp3↓, BAX↑, Bcl-2↓, Bcl-xL↓, IAP1↓, XIAP↓, survivin↓, MMP2↓, MMP9↓, CycB/CCNB1↓, CDC25↓, CDC25↓, Cyt‑c↑, MMP↓, RenoP↑, mTOR↓, MDM2↓, LC3II↑, ERK↓, COX2↓, MMP3↓, TGF-β↓, EMT↑, ROCK1↓, FAK↓, RAS↓, Rho↓, NF-kB↓, uPA↓, MMP1↓, MMP13↓, ChemoSen↑,

5631-

BCA,

Perspectives Regarding the Role of Biochanin A in Humans

Review,

Var,

Review,

AD,

*BioAv↓, *Inflam↓, AntiCan↑, *neuroP↑, chemoPv↑, Dose↝, *SOD↑, *MDA↓, *BAX↓, *HSP70/HSPA5↑, *AntiDiabetic↑, *Insulin↑, *TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *MMP9↓, *ROS↓, *PGE2↓, *BACE↓, *BioAv↑, P-gp⇅,

5633-

BCA,

Mechanisms Behind the Pharmacological Application of Biochanin-A: A review

Review,

Var,

Review,

AD,

*AntiDiabetic↑, *neuroP↑, *toxicity↓, *CYP19↓, p‑Akt↓, mTOR↓, TumCCA↑, P21↑, Casp3↑, Bcl-2↑, Apoptosis↑, E-cadherin↓, TumMeta↓, eff↑, GSK‐3β↓, β-catenin/ZEB1↓, RadioS↑, ROS↑, Casp1↑, MMP2↓, MMP9↓, EGFR↓, ChemoSen↑, PI3K↓, MMPs↓, Hif1a↓, VEGF↓, *ROS↓, *Obesity↓, *cardioP↑, *NRF2↑, *NF-kB↓, *Inflam↓, *lipid-P↓, *hepatoP↑, *AST↓, *ALP↓, *Bacteria↓, *neuroP↑, *SOD↑, *GPx↑, *AChE↓, *BACE↓, *memory↑, *BioAv↓,

2760-

BetA,

A Review on Preparation of Betulinic Acid and Its Biological Activities

Review,

Var,

Review,

Stroke,

AntiTum↑, Cyt‑c↑, Smad1↑, Sepsis↓, NF-kB↓, ICAM-1↓, MCP1↓, MMP9↓, COX2↓, PGE2↓, ERK↓, p‑Akt↓, *ROS↓, *LDH↓, *hepatoP↑, *SOD↑, *Catalase↑, *GSH↑, *AST↓, *ALAT↓, *RenoP↑, *ROS↓, *α-SMA↓,

4619-

Bor,

Using Boron Supplementation in Cancer Prevention and Treatment: A Review Article

Review,

Var,

Dose↝, Risk↓, *antiOx↓, *Inflam↓, ChemoSen↑, AntiCan↑, *PCNA↓, *ROS↓, other↝,

2776-

Bos,

Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities

Review,

Var,

*5LO↓, *TNF-α↓, *MMP3↓, *COX1↓, *COX2↓, *PGE2↓, *Th2↑, *Catalase↑, *SOD↑, *NO↑, *PGE2↑, *IL1β↓, *IL6↓, *Th1 response↓, *Th2↑, *iNOS↓, *NO↓, *p‑JNK↓, *p38↓, GutMicro↑, p‑Akt↓, GSK‐3β↓, cycD1/CCND1↓, Akt↓, STAT3↓, CSCs↓, AR↓, P21↑, DR5↑, CHOP↑, Casp3↑, Casp8↑, cl‑PARP↑, DNAdam↑, p‑RB1↓, FOXM1↓, TOP2↓, CDC25↓, p‑CDK1↓, p‑ERK↓, MMP9↓, VEGF↓, angioG↓, ROS↑, Cyt‑c↑, AIF↑, Diablo↑, survivin↓, ICAD↓, ChemoSen↑, SOX9↓, ER Stress↑, GRP78/BiP↑, cal2↓, AMPK↓, mTOR↓, ROS↓,

2775-

Bos,

The journey of boswellic acids from synthesis to pharmacological activities

Review,

Var,

Review,

AD,

Review,

PSA,

ROS↑, ER Stress↑, TumCG↓, Apoptosis↑, Inflam↓, ChemoSen↑, Casp↑, ERK↓, cl‑PARP↑, AR↓, cycD1/CCND1↓, VEGFR2↓, CXCR4↓, radioP↑, NF-kB↓, VEGF↓, P21↑, Wnt↓, β-catenin/ZEB1↓, Cyt‑c↑, MMP2↓, MMP1↓, MMP9↓, PI3K↓, MAPK↓, JNK↑, *5LO↓, *NRF2↑, *HO-1↑, *MDA↓, *SOD↑, *hepatoP↑, *ALAT↓, *AST↓, *LDH↑, *CRP↓, *COX2↓, *GSH↑, *ROS↓, *Imm↑, *Dose↝, *eff↑, *neuroP↑, *cognitive↑, *IL6↓, *TNF-α↓,

2768-

Bos,

Boswellic acids as promising agents for the management of brain diseases

Review,

Var,

Review,

AD,

Review,

Park,

*neuroP↑, *ROS↓, *cognitive↓, TumCP↓, TumCMig↓, TumMeta↓, angioG↓, Apoptosis↑, *Inflam↓, IL1↓, IL2↓, IL4↓, IL6↓, TNF-α↓, P53↑, Akt↓, NF-kB↓, DNAdam↑, Casp↑, COX2↓, MMP9↓, CXCR4↓, VEGF↓, *SOD↑, *Catalase↑, *GPx↑, *NRF2↑,

5744-

Buty,

PacT,

Oral sodium butyrate supplementation ameliorates paclitaxel-induced behavioral and intestinal dysfunction

in-vivo,

Var,

 BuNa dissolved in drinking water (0.23 mg/ml)

mice

chemoP↑, neuroP↑, Inflam↓, GutMicro↑, *ROS↓, Dose↝,

5743-

Buty,

Regulation of Intestinal Butyrate Transporters by Oxidative and Inflammatory Status

Review,

Var,

*GutMicro↑, *other↑, *Inflam↓, *ROS↓, AntiCan↑, HCAR2↑, HDAC↓,

5742-

Buty,

Butyrate: A Double-Edged Sword for Health?

Review,

Var,

HCAR2↑, Inflam↓, HDAC↓, *IFN-γ↓, *TNF-α↓, *IL1β↓, *IL6↓, *IL8↓, *IL10↑, *TNF-β↑, *NF-kB↓, *ROS↓, PPARγ↓, Weight↓,

5751-

CA,

Potential Therapeutic Implications of Caffeic Acid in Cancer Signaling: Past, Present, and Future

Review,

Var,

*antiOx↑, *chemoPv↑, ROS↑, MMP2↓, MMP9↓, BioAv↓, eff↑, *Inflam↓, AMPK↑, lipid-P↑, eff↑, ChemoSen↑, *memory↑, *ROS↓,

2019-

CAP,

Capsaicin: A Two-Decade Systematic Review of Global Research Output and Recent Advances Against Human Cancer

Review,

Var,

chemoPv↑, Ca+2↑, antiOx↑, *ROS↓, *MMP∅, *Cyt‑c∅, *Casp3∅, *eff↑, *Inflam↓, *NF-kB↓, *COX2↓, iNOS↓, TRPV1↑, i-Ca+2?, MMP↓, Cyt‑c↑, Bax:Bcl2↑, P53↑, JNK↑, PI3K↓, Akt↓, mTOR↓, LC3II↑, ATG5↑, p62↑, Fap1↓, Casp3↑, Apoptosis↑, ROS↑, MMP9↓, eff↑, eff↓, eff↑, selectivity↑, eff↑, ChemoSen↑,

5758-

CAPE,

PBG,

Caffeic acid phenethyl ester and therapeutic potentials

Review,

Var,

*antiOx↑, *Inflam↓, ChemoSen↑, chemoP↑, COX1↓, COX2↓, selectivity↑, NF-kB↓, RadioS↑, *ROS↓, *lipid-P↓,

5888-

CAR,

Therapeutic application of carvacrol: A comprehensive review

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Park,

*antiOx↑, *AntiCan↑, *AntiDiabetic↑, *cardioP↑, *Obesity↓, *hepatoP↑, *AntiAg↑, *Bacteria↓, *Imm↑, MMP2↓, MMP9↓, Apoptosis↓, MMP↓, ERK↓, PI3K↓, ALAT↓, *ROS↓, *Catalase↑, *SOD↑, *GPx↑, *AST↓, *LDH↓, *necrosis↓, ROS↑, TumCCA↑, CDK4↓, cycD1/CCND1↓, NOTCH↓, IL6↓, chemoP↑, *Pain↓, *neuroP↑, *TRPM7↓, *motorD↑, *NF-kB↓, *COX2↓, *MDA↓,

6018-

CGA,

Chlorogenic acid: a review on its mechanisms of anti-inflammation, disease treatment, and related delivery systems

Review,

Var,

Review,

RCC,

*BioAv↓, *Inflam↓, *TNF-α↓, *NO↓, *COX2↓, *PGE2↓, *NF-kB↓, *IL6↓, *IL1β↓, *TLR2↓, *MAPK↓, *NRF2↓, *HO-1↑, *NQO1↑, *cardioP↑, *neuroP↑, *SOD↑, *GSH↑, *ROS↓, *LDH↓, *MDA↓, *cognitive↑, *eff↑,

6017-

CGA,

Therapeutic Potential of Chlorogenic Acid in Chemoresistance and Chemoprotection in Cancer Treatment

Review,

Var,

AntiCan↑, *chemoP↑, TNF-α↓, COX2↓, IL6↓, eff↑, PD-L1↓, *cognitive↓, *Aβ↓, *TAC↑, *SOD↑, *eff↑, *eff↑, ChemoSen↑, tumCV↓, Apoptosis↑, ERK↓, chemoP↑, *GPx↑, *GSTs↑, *GSH↑, *SOD↑, *Catalase↑, *ROS↓, *lipid-P↓, *MDA↓, *Casp3↓, *HO-1↓, cardioP↑, radioP↑,

6016-

CGA,

Coffee Chlorogenic Acids Incorporation for Bioactivity Enhancement of Foods: A Review

Review,

Var,

Review,

AD,

Review,

Diabetic,

antiOx↑, *Bacteria↓, AntiCan↑, *Inflam↓, *cardioP↑, *AntiDiabetic↑, *GutMicro↑, *eff↑, *eff↑, *ROS↓, *IronCh↑, *neuroP↑, *AChE↓, *BChE↓, *chemoPv↑, *BioAv⇅,

6002-

CGA,

Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials

Review,

Var,

Review,

Diabetic,

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,

6001-

Chit,

Recent advances in engineering chitosan-based nanoplatforms in biotherapeutic multi-delivery for multi-targeted disease treatments: Promises and outlooks

Review,

Var,

HepG2

Review,

AD,

TumVol↓, toxicity↓, Half-Life↑, eff↑, selectivity↑, Dose↝, *BDNF↑, *NRF2↑, *ROS↓, *neuroP↑, *memory↑, *cognitive↑, *Obesity↓,

4481-

Chit,

Antioxidant Properties and Redox-Modulating Activity of Chitosan and Its Derivatives: Biomaterials with Application in Cancer Therapy

Review,

Var,

*BioAv↑, *toxicity↓, *antiOx↑, AntiCan↑, *Inflam↓, *ROS↓, *lipid-P↓, MDA↓, selectivity↑, MMP↓, ROS↑, TumCCA↑, MDA↑, GSH↓, ChemoSen↑,

6088-

CHOC,

Effect of chocolate on older patients with cancer in palliative care: a randomised controlled study

Trial,

Var,

eff↑, *ROS↓, *MDA↓, *GSH↑,

6086-

CHOC,

Cocoa and Chocolate in Human Health and Disease

Review,

Var,

*antiOx↑, *AntiDiabetic↑, *cognitive↑, *AntiAg↑, *AntiAg↑, *LDL↓, *HDL↑, *BP↓, *eff↓, *ROS↓,

6082-

CHOC,

Potential for preventive effects of cocoa and cocoa polyphenols in cancer

Review,

Var,

*ROS↓, Apoptosis↑, Inflam↓, TumCP↓, angioG↓, TumMeta↓, *Ca+2↓, *MMP∅, CYP1A1↑, PGE2↓, TumCCA↑, chemoPv↑,

2781-

CHr,

PBG,

Chrysin a promising anticancer agent: recent perspectives

Review,

Var,

PI3K↓, Akt↓, mTOR↓, MMP9↑, uPA↓, VEGF↓, AR↓, Casp↑, TumMeta↓, TumCCA↑, angioG↓, BioAv↓, *hepatoP↑, *neuroP↑, *SOD↑, *GPx↑, *ROS↓, *Inflam↓, *Catalase↑, *MDA↓, ROS↓, BBB↑, Half-Life↓, BioAv↑, ROS↑, eff↑, ROS↑, ROS↑, lipid-P↑, ER Stress↑, NOTCH1↑, NRF2↓, p‑FAK↓, Rho↓, PCNA↓, COX2↓, NF-kB↓, PDK1↓, PDK3↑, GLUT1↓, Glycolysis↓, mt-ATP↓, Ki-67↓, cMyc↓, ROCK1↓, TOP1↓, TNF-α↓, IL1β↓, CycB/CCNB1↓, CDK2↓, EMT↓, STAT3↓, PD-L1↓, IL2↑,

2782-

CHr,

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

Review,

Var,

Review,

Stroke,

Review,

Park,

*antiOx↑, *Inflam↓, *hepatoP↑, *neuroP↑, *BioAv↓, *cardioP↑, *lipidLev↓, *RenoP↑, *TNF-α↓, *IL2↓, *PI3K↓, *Akt↓, *ROS↓, *cognitive↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, VEGF↓, p‑STAT3↓, TumMeta↓, TumCP↓, eff↑, eff↑, IL1β↓, IL6↓, NF-kB↓, ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, ER Stress↑, Ca+2↑, TET1↑, Let-7↑, Twist↓, EMT↓, TumCCA↑, Casp3↑, Casp9↑, BAX↑, HK2↓, GlucoseCon↓, lactateProd↓, Glycolysis↓, SHP1↑, N-cadherin↓, E-cadherin↑, UPR↑, PERK↑, ATF4↑, eIF2α↑, RadioS↑, NOTCH1↑, NRF2↓, BioAv↑, eff↑,

2784-

CHr,

Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)

Review,

Var,

Apoptosis↑, TumCMig↓, *toxicity↝, ChemoSen↑, *BioAv↓, Dose↝, neuroP↑, *P450↓, *ROS↓, *HDL↑, *GSTs↑, *SOD↑, *Catalase↑, *MAPK↓, *NF-kB↓, *PTEN↑, *VEGF↑, ROS↑, MMP↓, Ca+2↑, selectivity↑, PCNA↓, Twist↓, EMT↓, CDKN1C↑, p‑STAT3↑, MMP2↓, MMP9↓, eff↑, cycD1/CCND1↓, hTERT/TERT↓, CLDN1↓, TumVol↓, OS↑, COX2↓, eff↑, CDK2↓, CDK4↓, selectivity↑, TumCCA↑, E-cadherin↑, HK2↓, HDAC↓,

2786-

CHr,

Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives

Review,

Var,

Apoptosis↑, TumCCA↑, angioG↓, TumCI↓, TumMeta↑, *toxicity↓, selectivity↑, chemoPv↑, *GSTs↑, *NADPH↑, *GSH↑, HDAC8↓, Hif1a↓, *ROS↓, *NF-kB↓, SCF↓, cl‑PARP↑, survivin↓, XIAP↓, Casp3↑, Casp9↑, GSH↓, ChemoSen↑, Fenton↑, P21↑, P53↑, cycD1/CCND1↓, CDK2↓, STAT3↓, VEGF↓, Akt↓, NRF2↓,

2788-

CHr,

Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of action

Review,

Var,

*neuroP↑, *Inflam↓, *ROS↓, NF-kB↓, *PCNA↓, *COX2↓, ChemoSen↑, Hif1a↓, angioG↓, *chemoPv↑, PDGF↓, *memory↑, *RenoP↑, *PPARα↑, *lipidLev↓, *hepatoP↑, *cardioP⇅, *BioAv↓,

2790-

CHr,

Chrysin: Pharmacological and therapeutic properties

Review,

Var,

*hepatoP↑, *neuroP↓, *ROS↓, *cardioP↑, *Inflam↓, eff↑, hTERT/TERT↓, cycD1/CCND1↓, MMP9↓, MMP2↓, TIMP1↑, TIMP2↑, BioAv↑, HK2↓, ROS↑, MMP↓, Casp3↑, ADP:ATP↑, Apoptosis↑, ER Stress↑, UPR↑, GRP78/BiP↝, eff↑, Ca+2↑,

1576-

Citrate,

Targeting citrate as a novel therapeutic strategy in cancer treatment

Review,

Var,

TCA↓, T-Cell↝, Glycolysis↓, PKM2↓, PFK2?, SDH↓, PDH↓, β-oxidation↓, CPT1A↓, FASN↑, Casp3↑, Casp2↑, Casp8↑, Casp9↑, cl‑PARP↑, Hif1a↓, GLUT1↓, angioG↓, Ca+2↓, ROS↓, eff↓, Dose↓, eff↑, Mcl-1↓, HK2↓, IGF-1R↓, PTEN↑, citrate↓, Dose∅, eff↑, eff↑, eff↑, eff↑,

4762-

CoQ10,

The role of coenzyme Q10 as a preventive and therapeutic agent for the treatment of cancers

Review,

Var,

*AntiCan↓, *ROS↓, chemoPv↑, TumCCA↑, Apoptosis↑, TumCP↓, angioG↓, MMPs↓, ChemoSen∅,

4768-

CoQ10,

Role of coenzymes in cancer metabolism

Review,

Var,

Risk↓, *ROS↓, AntiCan↑, TumMeta↓, ROS↑, TumCG↓, Apoptosis↑, TumMeta↓, Wnt↓, β-catenin/ZEB1↓, TumCG↓, selectivity↑, RadioS↑, ChemoSen↑, H2O2↓, MMP2↓, cardioP↑, ChemoSen∅, Dose↝,

4769-

CoQ10,

CoQ10 Is Key for Cellular Energy and Cancer Support

Review,

Var,

Risk↓, TumCG↓, angioG↓, TumCD↑, *toxicity↓, *BioAv↑, MMPs↓, Inflam↓, chemoP↑, cardioP↑, *ROS↓, *toxicity↝, Dose?,

4771-

CoQ10,

Coenzyme Q10 Protects Astrocytes from ROS-Induced Damage through Inhibition of Mitochondria-Mediated Cell Death Pathway

Review,

Var,

*ROS↓,

5780-

CRMs,

HCAs,

RES,

Sper,

ASA

Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential

Review,

Var,

*OS↑, *AntiAge↑, *cardioP↑, *neuroP↑, AntiCan↑, *TNF-α↓, *Weight↓, *BP↓, *Inflam↓, *Insulin↓, *ROS↓, *AMPK↑, *mTOR↓, *SIRT1↑, CRM↑,

Showing Research Papers: 1 to 50 of 158
Page 1 of 4 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 158

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Sepsis↓, 2,
Total Targets: 281

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 16, Catalase↑, 9, GPx↑, 7, GSH↑, 12, GSTs↑, 4, HDL↑, 2, HO-1↓, 1, HO-1↑, 3, Keap1↓, 1, lipid-P↓, 6, MDA↓, 9, MPO↓, 2, NQO1↑, 1, NRF2↓, 1, NRF2↑, 9, ROS?, 1, ROS↓, 47, ROS∅, 1, SOD↑, 15, SOD2↑, 1, TAC↑, 1, TBARS↓, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 4,

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1, Insulin↑, 1, MMP↑, 1, MMP∅, 2,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 3, AMPK↑, 3, AMPK⇅, 1, FAO↑, 1, glucose↓, 1, GlucoseCon↑, 1, H2S↑, 1, LDH↓, 6, LDH↑, 1, LDL↓, 1, lipidLev↓, 2, NADPH↑, 1, PPARα↑, 1, PPARα↝, 1, p‑PPARγ↓, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt?, 1, Akt↓, 3, BAX↓, 1, Casp↓, 1, Casp3↓, 1, Casp3∅, 1, Cyt‑c∅, 1, iNOS↓, 4, JNK↓, 1, p‑JNK↓, 1, MAPK↓, 2, necrosis↓, 1, p38↓, 1,

Transcription & Epigenetics ⓘ

other↑, 2,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

DNArepair↑, 1, PCNA↓, 2,

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1, PI3K↓, 3, PI3K↑, 1, PTEN↑, 1, STAT3↓, 1, TRPM7↓, 1,

Migration ⓘ

5LO↓, 2, AntiAg↑, 3, Ca+2↓, 2, MMP2↓, 1, MMP3↓, 1, MMP9↓, 2, TRPC1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2, NO↓, 3, NO↑, 1, VEGF↓, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 3,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 12, CRP↓, 1, IFN-γ↓, 1, IL10↑, 2, IL18↓, 1, IL1β↓, 6, IL2↓, 1, IL6↓, 9, IL8↓, 2, Imm↑, 3, Inflam↓, 20, NF-kB↓, 13, PGE2↓, 5, PGE2↑, 1, Th1 response↓, 1, Th2↑, 2, TLR2↓, 2, TLR4↓, 1, TNF-α↓, 11, TNF-β↑, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 3, BChE↓, 1, BDNF↑, 2,

Protein Aggregation ⓘ

Aβ↓, 2, BACE↓, 2, β-Amyloid↓, 1,

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 8, BioAv↑, 4, BioAv⇅, 1, BioAv↝, 4, ChemoSen↑, 1, Dose↑, 1, Dose↝, 2, eff↓, 1, eff↑, 11, Half-Life↓, 1, Half-Life↝, 4, P450↓, 1,

Clinical Biomarkers ⓘ

ALAT↓, 3, ALP↓, 1, AST↓, 5, BG↓, 1, BP↓, 4, creat↓, 1, CRP↓, 1, GutMicro↑, 5, IL6↓, 9, LDH↓, 6, LDH↑, 1,

Functional Outcomes ⓘ

AntiAge↑, 2, AntiCan↓, 1, AntiCan↑, 2, AntiDiabetic↑, 7, cardioP↓, 1, cardioP↑, 12, cardioP⇅, 1, chemoP↑, 1, chemoPv↑, 5, cognitive↓, 2, cognitive↑, 8, hepatoP↑, 14, memory↑, 7, motorD↑, 2, neuroP↓, 1, neuroP↑, 22, Obesity↓, 3, OS↑, 1, Pain↓, 1, RenoP↑, 4, toxicity↓, 5, toxicity↝, 2, Weight↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 4,
Total Targets: 156

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

9 Quercetin
9 Thymoquinone
8 Fisetin
7 Propolis -bee glue
7 Curcumin
7 Lycopene
6 Chrysin
6 Rosmarinic acid
5 Baicalein
5 Resveratrol
5 Silymarin (Milk Thistle) silibinin
4 Chlorogenic acid
4 Coenzyme Q10
4 Chemotherapy
4 Hydrogen Gas
4 Honokiol
4 Selenite (Sodium)
3 Alpha-Lipoic-Acid
3 Radiotherapy/Radiation
3 Boswellia (frankincense)
3 Butyrate
3 Chocolate
3 Luteolin
3 Melatonin
3 Selenium
3 Selenium NanoParticles
3 Vitamin C (Ascorbic Acid)
2 Allicin (mainly Garlic)
2 Ashwagandha(Withaferin A)
2 Baicalin
2 Biochanin A
2 chitosan
2 EGCG (Epigallocatechin Gallate)
2 Oleuropein
2 Pterostilbene
2 Sulforaphane (mainly Broccoli)
2 Urolithin
1 Apigenin (mainly Parsley)
1 Astaxanthin
1 Berberine
1 Betulinic acid
1 Boron
1 Paclitaxel
1 Caffeic acid
1 Capsaicin
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Carvacrol
1 Citric Acid
1 Calorie Restriction Mimetics
1 Hydroxycinnamic-acid
1 Spermidine
1 Aspirin -acetylsalicylic acid
1 Cisplatin
1 diet Ketogenic
1 Oxygen, Hyperbaric
1 diet Methionine-Restricted Diet
1 Graviola
1 Juglone
1 Magnolol
1 Moringa oleifera
1 HydroxyTyrosol
1 Oleocanthal
1 Phenethyl isothiocyanate
1 Piperine
1 Salvia officinalis
1 Shikonin
1 Thymol-Thymus vulgaris
1 Vitamin D3
1 Vitamin K2

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:26  Cells:%  prod#:%  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

ROS Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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