Lycopene / ROS Cancer Research Results

Lyco, Lycopene: Click to Expand ⟱
Features:
Lycopene is a naturally occurring carotenoid found predominantly in tomatoes and other red fruits and vegetables.

Lycopene — a highly lipophilic, acyclic C40 carotenoid (tetraterpene) responsible for the red coloration of tomatoes, watermelon, pink grapefruit, guava, and related foods. It is a non-provitamin-A carotenoid and dietary bioactive rather than an approved anticancer drug. Standard abbreviations include Lyc and LYCO. Tomatoes and processed tomato products are the dominant dietary sources in many populations. Lycopene isomers and oxidative metabolites may differ biologically; circulating and tissue lycopene contains a substantially larger cis-isomer fraction than typical raw tomato sources.

Primary mechanisms (ranked):

  1. Redox modulation: strong singlet-oxygen quenching and antioxidant activity predominate physiologically, while some cancer models show context-dependent mitochondrial ROS generation and pro-oxidant apoptosis.
  2. IGF-1 / PI3K / AKT / mTOR growth signaling suppression, contributing to reduced proliferation and increased apoptosis in multiple experimental cancer models.
  3. Mevalonate / HMG-CoA reductase / Ras signaling suppression, reducing cholesterol synthesis, protein prenylation, Ras membrane localization, and downstream proliferative signaling.
  4. Cell-cycle inhibition through cyclin D1 and other cyclins/CDKs with increased p21/p27 and G0/G1 or other model-dependent arrest.
  5. Intrinsic apoptosis modulation through increased Bax:Bcl-2 ratio, mitochondrial dysfunction, cytochrome-c release, and caspase activation in responsive cancer models.
  6. Anti-inflammatory signaling through suppression of NF-κB, COX-2, IL-6, TNF-α and related inflammatory mediators.
  7. Migration, invasion and EMT suppression involving FAK, MMP2/MMP9, β-catenin, Rho-family signaling and epithelial-mesenchymal transition pathways.
  8. Anti-angiogenic signaling involving VEGF and HIF-1α suppression in selected experimental systems.
  9. NRF2-dependent antioxidant defense is important primarily in normal-cell protection and chemoprevention models; its direction in established cancer is context-dependent rather than uniformly beneficial.

Bioavailability / PK relevance: Oral absorption is formulation- and food-matrix-dependent. Lycopene is lipophilic and incorporation into mixed micelles is improved by dietary fat, disruption of the tomato matrix by processing, and some cis-rich formulations. Human isotope studies indicate substantial interindividual variability and postabsorptive trans-to-cis isomerization. Plasma/tissue persistence is relatively long compared with many phytochemicals, but reported half-life depends strongly on the kinetic model and whether endogenous/background lycopene is being measured.
- tangerine tomato juice has a marked 8.5-fold increase in lycopene bioavailability compared to red tomato juice
- taking with olive oil improves bioavailability. - Lycopene from fresh and unprocessed tomatoes is poorly absorbed by humans. Absorption of lycopene is higher from processed foods such as tomato paste and tomato juice heated in oil.
- cis-isomers of lycopene are more bioavailable than trans-lycopene probably because cis-isomers are more soluble in bile acid micelles.(tomato-based foods contain mainly all-trans-lycopene)
>

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 1–20 µM lycopene, with several mechanistic studies clustering near 2.5–10 µM. Human circulating concentrations after dietary or supplemental intake are generally much lower than the upper concentrations used experimentally; therefore mechanisms demonstrated at high micromolar concentrations should not automatically be assumed achievable in tumors after ordinary oral supplementation. Formulation, food matrix, tissue accumulation and lycopene metabolites further complicate direct concentration comparisons.

Clinical evidence status: RCT / small human / observational evidence, but not established anticancer treatment. Human studies are strongest for biomarker modulation and prostate-related research, while prospective epidemiology generally associates higher dietary or circulating lycopene with modestly lower cancer risk. Trials have not established lycopene as a replacement for standard cancer therapy. Lycopene is used as a food constituent and dietary supplement; FDA GRAS determinations for specified food uses are not anticancer drug approvals.


Antioxidant Properties:
-Lycopene is a powerful antioxidant. It helps neutralize free radicals, which can reduce oxidative stress—a factor implicated in cancer development. Possible concern about interfering with chemotherapy and radiation therapy. However this review disagrees.
Inflammation Reduction:
-Some studies suggest that lycopene may help lower levels of inflammation, another process linked to cancer progression

At supraphysiological or extremely high concentrations, lycopene may have the potential to switch from an antioxidant to a prooxidant role
-The prooxidant effect of lycopene has been observed under conditions of high oxygen tension. In vitro studies have suggested that in environments with elevated oxygen levels, lycopene might promote rather than neutralize the production of reactive oxygen species (ROS).
-The presence of metal ions (such as iron or copper) in the environment can catalyze reactions where antioxidants, including lycopene, contribute to oxidative processes. These metals can interact with lycopene, potentially leading to the formation of radicals.

The mevalonate pathway produces cholesterol and a variety of isoprenoids, which are important for maintaining cell membrane integrity, protein prenylation, and other essential cellular functions.
-One of the primary enzymes in this pathway is HMG-CoA reductase (3-hydroxy-3-methylglutaryl-coenzyme A reductase), which is the target of statin drugs used for lowering cholesterol. Some studies suggest that lycopene might downregulate the activity of HMG-CoA reductase or other enzymes in the mevalonate pathway. By doing so, lycopene could potentially reduce the synthesis of cholesterol and isoprenoids that are necessary for rapid cell proliferation—an especially relevant aspect in cancer cells.

Lycopene typically used in a 100mg/day range for cancer (inhibition of the the Melavonate Pathway)
-also has antiplatelet aggregation capability.

-Note half-life 16–20 days (other ref 5 days).
BioAv Heat processing, especially when combined with a small amount of fat, significantly enhances lycopene’s bioaccessibility and absorption. (20% under optimal conditions)
Pathways:
- ROS usually goes down, but may go up or down depending on dose and environment. Lycopene may also be modified to be a "oxdiative product" which may change the behaviour.
- Raises AntiOxidant defense in Normal Cells: ROS↓">ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : EMT↓, MMPs↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : EZH2↓, P53↑, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Integrins↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Lycopene Mechanistic Ranking

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Redox and reactive oxygen species ROS ↓ or ↑ (context-dependent); mt-ROS ↑ in selected models ROS ↓; lipid peroxidation ↓ R–G Redox modulation Antioxidant behavior predominates physiologically, but pro-oxidant mitochondrial ROS-mediated apoptosis occurs in some cancer models. Direction depends on cell type, oxygen tension, dose and lycopene oxidation state.
2 IGF-1 / PI3K / AKT / mTOR IGF-1 signaling ↓; PI3K ↓; AKT ↓; mTOR ↓ ↔ or protective modulation (context-dependent) R–G Growth and survival signaling ↓ One of the most recurrent cancer-relevant signaling clusters; effects vary by tumor model.
3 Mevalonate / HMG-CoA reductase / Ras HMG-CoA reductase ↓; cholesterol synthesis ↓; membrane Ras ↓ LDL/cholesterol regulation ↓ (context-dependent) G Growth signaling and prenylation ↓ Mechanistically important but demonstrated mainly preclinically. Mevalonate can reverse lycopene-induced growth inhibition in experimental cancer cells.
4 Cell-cycle machinery Cyclin D1 ↓; cyclin E ↓; CDK2 ↓; CDK4 ↓; p21 ↑; p27 ↑; arrest ↑ ↔ (generally spared) G Proliferation ↓ Frequently reported downstream consequence of growth-factor, Ras and AKT pathway suppression.
5 Mitochondrial apoptosis Bax:Bcl-2 ↑; MMP ↓; Cyt-c ↑; caspase-9 ↑; caspase-3 ↑; apoptosis ↑ Mitochondrial damage ↓; apoptosis ↓ under oxidative injury R–G Selective death signaling Direction differs markedly by malignant versus stressed normal-cell context.
6 NF-κB inflammatory signaling NF-κB ↓; COX-2 ↓; IL-6 ↓; TNF-α ↓ NF-κB ↓; inflammatory cytokines ↓ R–G Inflammation ↓ Supported across cancer and non-cancer inflammatory models; likely partly secondary to redox and kinase modulation.
7 EMT / FAK / MMP invasion axis EMT ↓; FAK ↓; MMP2 ↓; MMP9 ↓; migration ↓; invasion ↓ ↔ (context-dependent) G Migration and invasion ↓ Relevant mainly to preclinical metastatic phenotypes rather than demonstrated clinical antimetastatic efficacy.
8 Wnt / β-catenin / STAT3 Wnt ↓; β-catenin ↓; JAK1 ↓; STAT3 ↓ ↔ (context-dependent) G Proliferative transcription ↓ Observed in several epithelial cancer models but not established as a universal primary target.
9 VEGF / HIF-1α angiogenesis VEGF ↓; HIF-1α ↓; angiogenesis ↓ ↔ or angiogenic signaling ↓ (context-dependent) G Angiogenesis ↓ Predominantly preclinical evidence.
10 NRF2 / antioxidant response NRF2 ↑ or ↓ (context-dependent) NRF2 ↑; HO-1 ↑; NQO1 ↑; SOD ↑; GSH defense ↑ R–G Stress defense ↑ NRF2 activation is well supported in protective normal-tissue models. In established cancer, NRF2 biology is dual-sided and should not be represented as uniformly anticancer.
11 DNA damage and genomic protection DNA damage ↑ or ↓ (model-dependent); p53 ↑ Oxidative DNA damage ↓ G Context-dependent genomic modulation Normal-cell chemoprevention and cancer-cell killing can produce opposite apparent directions.
12 Glycolysis and metabolic signaling Glycolysis ↓ (limited evidence); c-Myc ↓; G6PD ↓ ↔ G Metabolic growth support ↓ Evidence is substantially less developed than for AKT, cell cycle or redox pathways; should remain secondary.
13 Chemosensitization Sensitivity ↑ (drug- and model-dependent) Chemotoxicity may ↓ in protective models G Adjunct response modulation Preclinical sensitization has been reported, including androgen-axis therapies; simultaneous cytoprotection is also reported with some cytotoxic agents, so interaction cannot be generalized.
14 Radiosensitivity and radioprotection ↔ or sensitivity ↑ (model-dependent) Radioprotection ↑ in some models G Context-dependent radiation interaction Evidence supports both antioxidant radioprotection and experimental radiosensitization depending on system; clinical significance remains uncertain.
15 Clinical Translation Constraint Oral tumor exposure uncertain Generally well tolerated at nutritional and commonly studied supplemental exposure G Translation limited Low and variable oral bioavailability, food-matrix effects, nonlinear dose-exposure relationships, uncertain tumor concentrations, and limited adequately powered cancer RCTs constrain translation of high-concentration in-vitro mechanisms.

TSF: P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer’s disease relevance: Lycopene has meaningful preclinical AD relevance but no established clinical efficacy. Cell and animal models report reduced oxidative stress and neuroinflammation, improved mitochondrial function, suppression of BACE1 and amyloidogenic signaling, reduced Aβ burden, attenuation of tau hyperphosphorylation, and preservation of BDNF/synaptic signaling. Human evidence remains insufficient to classify lycopene as an AD treatment.

Translation status: Preclinical only for disease-modifying AD mechanisms. Computational, cellular, rodent and formulation studies support biological plausibility, but clinical supplementation studies have not demonstrated prevention or treatment of Alzheimer’s disease.

Lycopene in Alzheimer’s Disease Models

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Oxidative stress / NRF2 ROS ↓; NRF2 ↑; antioxidant defense ↑ Oxidative neuronal injury ↓ One of the most consistent effects in cellular and animal neurotoxicity models.
2 Amyloid / BACE1 BACE1 ↓; Aβ ↓ Amyloidogenic processing ↓ Supported experimentally; no demonstrated disease-modifying effect in humans.
3 Neuroinflammation / NF-κB NF-κB ↓; TNF-α ↓; IL-1β ↓; IL-6 ↓ Neuroinflammation ↓ Reported in several Aβ and inflammatory animal models.
4 Mitochondrial function mt-ROS ↓; MMP preserved; mitochondrial damage ↓ Bioenergetic integrity ↑ Consistent with antioxidant and anti-apoptotic neuronal effects.
5 Tau phosphorylation Hyperphosphorylated tau ↓ Tau pathology ↓ Demonstrated in transgenic mouse models; human relevance remains unproven.
6 BDNF / synaptic plasticity BDNF ↑; TrkB signaling ↑ Synaptic resilience ↑ Preclinical evidence suggests preservation of learning/memory pathways.
7 Neuronal apoptosis Bax:Bcl-2 ↓; Cyt-c ↓; caspase-3 ↓ Neuronal survival ↑ Predominantly secondary to redox, mitochondrial and inflammatory modulation.


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)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

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

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

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

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

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

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

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

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




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



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






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






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






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






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






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






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






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






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






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






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






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






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






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






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






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






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






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






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






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






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






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






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






ROS">Piperine
+±[D][F]ROS-secondary






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






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






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






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






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
1566- betaCar,  Lyco,    Antioxidant and pro-oxidant effects of lycopene in comparison with beta-carotene on oxidant-induced damage in Hs68 cells
- in-vitro, Nor, HS68
*ROS↑, *ROS⇅, *Dose↝,
4797- Lyco,    A mechanistic updated overview on lycopene as potential anticancer agent
- Review, Var, NA
AntiCan↑, antiOx↓, Apoptosis↑, TumCP↓, TumCCA↑, Risk↓, ROS↓, SOD↑, Catalase↑, GSTs↑, ARE↑, NRF2↑, cycD1/CCND1↓, cycE/CCNE↑, CDK2↑, p27/CDKN1B↑, BAX↑, Bcl-2↓, P53↑, ChemoSen↑,
4796- Lyco,    The Anti-proliferation Effects of Lycopene on Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, Nor, MCF10
TumCG↓, selectivity↑, *BioAv↑, *antiOx↑, *ROS↓, Risk↓, *cardioP↑,
4794- Lyco,    Anticancer Effect of Lycopene in Gastric Carcinogenesis
- Review, GC, NA
*AntiCan↑, *ROS↓, *GSH↑, *GPx↑, *GSTs↑, TumCG↓, Apoptosis↑, ERK↓, Bcl-2↓, BAX↑, Cyt‑c↑, TumCCA↑, *DNAdam↓,
4793- Lyco,    Lycopene treatment inhibits activation of Jak1/Stat3 and Wnt/β-catenin signaling and attenuates hyperproliferation in gastric epithelial cells
- in-vitro, GC, AGS
antiOx↑, AntiCan↑, ROS↓, JAK1↓, STAT3↓, Wnt↓, β-catenin/ZEB1↓, cMyc↓, cycE/CCNE↓, TumCP↓, Risk↓,
4792- Lyco,    A Comprehensive Review on the Molecular Mechanism of Lycopene in Cancer Therapy
- Review, Var, NA
*AntiCan↑, *antiOx↑, Inflam↓, Wnt↓, β-catenin/ZEB1↓, *ROS↓, BioAv↑, ROS↓, Risk↓, PGE2↓, COX2/PTGS2↓, p‑ERK↓, P21↑, MMP7↓, MMP9↓, ChemoSen↑, Synergy↑,
4790- Lyco,    Role of Lycopene in the Control of ROS-Mediated Cell Growth: Implications in Cancer Prevention
- Review, Var, NA
*antiOx↑, *ROS⇅, TumCP↓, AP-1↓, eff↓,
4789- Lyco,    Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
- in-vitro, AD, SH-SY5Y
*antiOx↑, *ROS↓, *NF-kB↓, *neuroP↑, *MMP↓, *mtDam↓, *OCR↓,
4801- Lyco,    Lycopene in the Prevention of Cardiovascular Diseases
- Review, CardioV, NA
*BioAv↝, *cardioP↑, *BioAv↑, *BioAv↑, *antiOx↑, *ROS↓, *ARE↑, *SOD↑, *Catalase↑, *GPx↑, *lipid-P↓, *COX2/PTGS2↓, *Inflam↓, *IL1β↓, *IL6↓, *IL8↑, *TNF-α↓, *NF-kB↓, *BP↓,
4785- Lyco,    The Protective Anticancer Effect of Natural Lycopene Supercritical CO2 Watermelon Extracts in Adenocarcinoma Lung Cancer Cells
- in-vitro, Lung, A549
ROS↑, NF-kB↑, Apoptosis↑,
4784- Lyco,    Protective effects of lycopene in cancer, cardiovascular, and neurodegenerative diseases: An update on epidemiological and mechanistic perspectives
- Review, Diabetic, NA - Review, CardioV, NA
*antiOx↑, *IL8↓, *IL6↓, *IL1↓, *NF-kB↓, Inflam↓, cycD1/CCND1↓, MMP2↓, MMP9↓, Bcl-2↓, NF-kB↓, *Nrf1↑, *antiOx↑, *BDNF↑, *neuroP↑, *cardioP↑, ROS↑, Dose↝,
4782- Lyco,    New Insights into Molecular Mechanism behind Anti-Cancer Activities of Lycopene
- Review, Var, NA
AntiCan↑, TumCP↓, TumCMig↓, TumCI↓, TumCA↓, ROS↓, MMP2↓, MMP7↓, MMP9↓, VEGF↓, E-cadherin↑, TIMP1↑, TIMP2↑, BioAv↝, *IL12↓, *TNF-α↓, *IL1↓, *IL1β↓, *IL6↓, COX2/PTGS2↓, iNOS↓, *radioP↑, NF-kB↓, survivin↓, Casp3↑, Bax:Bcl2↑,
4781- Lyco,  5-FU,  Chemo,  Cisplatin,    Antioxidant and anti-inflammatory activities of lycopene against 5-fluorouracil-induced cytotoxicity in Caco2 cells
- in-vitro, Colon, Caco-2
chemoP↑, Inflam↓, COX2/PTGS2↓, IL1β↓, IL6↓, TNF-α↓, ROS↑, ChemoSen↑, SOD↓,
4779- Lyco,    Lycopene Inhibits Reactive Oxygen Species-Mediated NF-κB Signaling and Induces Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, PANC1
ROS↓, NF-kB↓, tumCV↓, Casp3↑, Apoptosis↑, OCR↓, MMP↓, CIP2A↓, survivin↓, Casp3↑, Bax:Bcl2↑,
4778- Lyco,    Lycopene exerts cytotoxic effects by mitochondrial reactive oxygen species–induced apoptosis in glioblastoma multiforme
- in-vitro, GBM, GBM8401
BBB↑, Apoptosis↑, TumCP↑, P53↑, CycB/CCNB1↓, cycD1/CCND1↓, TumCCA↓, mt-ROS↑, TumCG↓,
4777- Lyco,    Lycopene Inhibits Activation of Epidermal Growth Factor Receptor and Expression of Cyclooxygenase-2 in Gastric Cancer Cells
- in-vitro, GC, AGS
*antiOx↑, tumCV↓, DNAdam↑, Apoptosis↑, cl‑Casp3↑, cl‑Casp9↑, Bax:Bcl2↑, ROS↓, NF-kB↓, COX2/PTGS2↓, EGFR↓, p38↓,
4230- Lyco,    Supplementation of lycopene attenuates oxidative stress induced neuroinflammation and cognitive impairment via Nrf2/NF-κB transcriptional pathway
- in-vivo, AD, NA
*BDNF↑, *antiOx↑, *Inflam↓, *HO-1↑, *NQO1↑, *IL1β↓, *TNF-α↓, *ROS↓, *NRF2↑, *cognitive↑, *BBB↑,
8421- Lyco,    Lycopene: Sojourn from kitchen to an effective therapy in Alzheimer's disease
- Review, AD, NA
*neuroP↑, *antiOx↑, *Inflam↓, *AntiMyl↑, *ROS↓, *MMP↑, *NGF↑, *BDNF↑, *VEGF↑, *Aβ42↓, *PI3K↑, *Akt↑, *NRF2↑, *lipid-P↓, *GSH↑, *Catalase↑, *SOD↑, *cognitive↑, *Learn↑, *memory↑, *APP↓, *BACE/β-secretase↓, *ADAM10↑, *NF-kB↓, *AChE↓, *MAOA↓, *BioAv↝,
8416- Lyco,    Lycopene alleviates cognitive dysfunctions in an Alzheimer's disease rat model via suppressing the oxidative and neuroinflammatory signaling
- in-vivo, AD, NA
*Inflam↓, *ROS↓, *Dose↝, *Aβ42↓, *IL1β↓, *TNF-α↓, *MDA↓, *Ach↑, *MAOA↓, *LDH↓, *AChE↓, *NRF2↑, *5HT↑, *TGF-β1↑, *IL10↑, *Ki-67↓, *PCNA↓,
8414- Lyco,    Exploring the Therapeutic Potential of Lycopene: Mechanisms, Biological Activities, and Health Benefits
- Review, Var, NA - Review, AD, NA
*ROS↓, *Inflam↓, *hepatoP↑, *cardioP↑, *neuroP↑, *AntiArt↑, *Obesity↓, *Wound Healing↑, *BioAv↑, *GSTs↑, *Trx1↑, *SOD↑, *Catalase↑, *ALAT↓, *LDH↓, *AST↓, *MDA↓, *cognitive↑, *memory↑, *NeuroI↓, *Aβ↓, *LRP1↑, *RAGE↓, *NRF2↑, *HO-1↑, tumCV?, Bax:Bcl2↑, DNAdam↑, Apoptosis↑, β-catenin/ZEB1↓, cMyc↓, cycD1/CCND1↓, ROS↓, TumCCA↑, Akt↓, *Synergy↑, *MDA↓, *NF-kB↓, *TGF-β↓, *Casp3↓, *Catalase↑, *GSH↑, *Bcl-2↑, *IL10↑, *MUC1↑, *IBI↑, *RenoP↑, *ChemoSen↑, *Synergy↑, *Synergy↑, *BMD↑,
8407- Lyco,    Lycopene induces cell growth inhibition by altering mevalonate pathway and Ras signaling in cancer cell lines
- in-vitro, Pca, LNCaP
CholSyn↓, HMGCR↓, RAS↓, NF-kB↓, ROS↓, p‑Jun↓, TumCCA↑, Apoptosis↑, cycD1/CCND1↓, p‑Akt↓, P21↑, p27/CDKN1B↑, P53↑, Bax:Bcl2↑,
4803- Lyco,    Enhanced cytotoxic and apoptosis inducing activity of lycopene oxidation products in different cancer cell lines
- in-vitro, Pca, PC3 - in-vitro, BC, MCF7 - in-vitro, Melanoma, A431 - in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
tumCV↓, GSH↓, MDA↑, ROS↑, Apoptosis↑,
4228- Lyco,    A review for the pharmacological effect of lycopene in central nervous system disorders
- Review, AD, NA - Review, Park, NA
*cognitive↑, *memory↑, *Inflam↓, *Apoptosis↓, *ROS↓, *neuroP↑, *NF-kB↓, *JNK↓, *NRF2↑, *BDNF↑, *MDA↓, *GPx↑,
1716- Lyco,    Anti-inflammatory Activity of β-Carotene, Lycopene and Tri-n-butylborane, a Scavenger of Reactive Oxygen Species
- in-vitro, AML, RAW264.7
antiOx↑, lipid-P↓, ROS↑, Dose↑,
3264- Lyco,    Pharmacological potentials of lycopene against aging and aging‐related disorders: A review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*antiOx↑, *ROS↓, *SOD↑, *Catalase↑, *GSH↑, *GSTs↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *iNOS↓, *NO↓, *TAC↑, *NOX4↓, *Inflam↓, *IL1↓, *IL6↓, *IL8↓, *IL1β↓, *TNF-α↓, *TLR2↓, *TLR4↓, *VCAM-1↓, *ICAM-1↓, *STAT3↓, *NF-kB↓, *ERK↓, *BP↓, ROS↓, PGE2↓, cardioP↑, *neuroP↑, *creat↓, *RenoP↑, *CRM↑,
3262- Lyco,    Lycopene inhibits matrix metalloproteinase-9 expression and down-regulates the binding activity of nuclear factor-kappa B and stimulatory protein-1
- in-vitro, adrenal, SK-HEP-1
TumCI↓, MMP9↓, NF-kB↓, Sp1/3/4↓, IGF-1R↓, i-ROS↓,
3261- Lyco,    Lycopene and Vascular Health
- Review, Stroke, NA
*Inflam↓, *antiOx↑, *AntiAg↑, *cardioP↑, *SOD↑, *Catalase↑, *ROS↓, *mtDam↓, *cardioP↑, *NF-kB↓, *NO↓, *COX2/PTGS2↓, *LDL↓, *Synergy↑, *ER Stress↓, *BioAv↑, *Synergy↑, *MMPs↓, *COX2/PTGS2↓, *RAGE↓,
3260- Lyco,    Lycopene in human health
- Review, Nor, NA
*BioAv↝, *BioAv↓, *ROS⇅, *BioAv↝,
1721- Lyco,  RES,  VitC,    Lycopene, resveratrol, vitamin C and FeSO4 increase damage produced by pro-oxidant carcinogen 4-nitroquinoline-1-oxide in Drosophila melanogaster: Xenobiotic metabolism implications.
- in-vitro, Pca, PC3 - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF7 - in-vitro, Liver, HepG2
ROS↑,
1720- Lyco,    Antioxidant and Pro-oxidant Activities of Carotenoids
- Review, Nor, NA
ROS↑,
1719- Lyco,    Lycopene for the prevention and treatment of prostate disease.
- Review, Var, NA
ROS⇅,
1718- Lyco,    The role of carotenoids in the prevention of human pathologies
- Review, Var, NA
ROS⇅, ROS↑,
1717- Lyco,    Potential Role of Carotenoids as Antioxidants in Human Health and Disease
- Review, Var, NA
antiOx↑, ROS⇅, ROS↑,
1715- Lyco,    Pro-oxidant Actions of Carotenoids in Triggering Apoptosis of Cancer Cells: A Review of Emerging Evidence
- Review, Var, NA
antiOx↑, ROS↑, ChemoSen↑, selectivity↑, eff↓, Casp3↑, Casp7↑, Casp9↑, P53↑, BAX↑, DNAdam↑, mtDam↑, Synergy↑,
1713- Lyco,    Lycopene: A Potent Antioxidant with Multiple Health Benefits
- Review, Nor, NA
*antiOx↑, *ROS⇅, *Dose↝, *eff↑, *LDL↓, *RenoP↑, *Inflam↓, neuroP↑, Rho↓,
1712- Lyco,    Lycopene Protects against Smoking-Induced Lung Cancer by Inducing Base Excision Repair
- in-vitro, Lung, A549
ROS↓, ROS↑, eff↑,
1711- Lyco,    Nutritional Importance of Carotenoids and Their Effect on Liver Health: A Review
- Review, Var, NA
ROS↑, Dose↓, Dose↑, antiOx↑, P450↓, TNF-α↓, IL1β↓, IL12↓,
1710- Lyco,    Lycopene: A Natural Arsenal in the War against Oxidative Stress and Cardiovascular Diseases
- Review, CardioV, NA
antiOx↓, ROS↓, BP↓, LDL↓, *toxicity∅, eff↑, ROS↑, *Half-Life↑, *BioAv↓, *BioAv↑, *antiOx↑,
1013- Lyco,    Lycopene induces apoptosis by inhibiting nuclear translocation of β-catenin in gastric cancer cells
- in-vitro, GC, AGS
Apoptosis↑, DNAdam↑, Bax:Bcl2↑, ROS↓, β-catenin/ZEB1↓, p‑GSK‐3β↓, APC↑, β-TRCP↑, cMyc↓, cycD1/CCND1↓,
3828- Lyco,    Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer's disease
- in-vitro, AD, M146L
*ROS↓, *PI3K↑, *Akt↑, *NRF2↓, *antiOx↑, *BACE/β-secretase↓, *MDA↓,
3533- Lyco,  Chemo,    Lycopene and chemotherapy toxicity
- Review, Var, NA
*ROS↓, *antiOx↑, *chemoP↑, *Inflam↓,
3532- Lyco,    Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer’s disease
- in-vitro, AD, NA
*ROS↓, *PI3K↑, *Akt↑, *NRF2↑, *antiOx↑, *Aβ↓, *Apoptosis↓, *neuroP↑,
3531- Lyco,    Lycopene attenuates the inflammation and apoptosis in aristolochic acid nephropathy by targeting the Nrf2 antioxidant system
- in-vivo, Nor, NA
*NRF2↑, *HO-1↑, *NQO1↑, *ROS↓, *mtDam↓, *Bcl-2↑, *BAX↓, *Casp9↓, *Casp3↓, *Apoptosis↓, *RenoP↑, *lipid-P↓, *SOD↑, *GPx↑, *Inflam↓, *TNF-α↓, *IL6↓, *IL10↓,
3530- Lyco,    Lycopene Scavenges Cellular ROS, Modulates Autophagy and Improves Survival through 7SK snRNA Interaction in Smooth Muscle Cells
- in-vitro, Stroke, NA
*ROS↓, *antiOx↑, *TNF-α↓,
3529- Lyco,    The antioxidant and anti-inflammatory properties of lycopene in mice lungs exposed to cigarette smoke
- in-vivo, Nor, NA
*antiOx↑, *Inflam↓, *ROS↓, *TNF-α↓, *IFN-γ↓, IL10↓,
3528- Lyco,    The Importance of Antioxidant Activity for the Health-Promoting Effect of Lycopene
- Review, Nor, NA - Review, AD, NA - Review, Park, NA
*antiOx↑, *ROS↓, *BioAv↝, *Half-Life↑, *BioAv↓, *BioAv↑, *cardioP↑, *neuroP↑, *H2O2↓, *VitC↑, *VitE↑, *GPx↑, *GSH↑, *MPO↓, *GSTs↓, *SOD↑, *NF-kB↓, *IL1β↓, *IL6↓, *IL10↑, *MAPK↓, *Akt↓, *COX2/PTGS2↓, *TNF-α↓, *TGF-β1↑, *NO↓, *GSR↑, *NRF2↑, *HO-1↑, *TAC↑, *Inflam↓, *BBB↑, *neuroP↑, *memory↑,
4229- Lyco,    Implicating the role of lycopene in restoration of mitochondrial enzymes and BDNF levels in β-amyloid induced Alzheimer׳s disease
- in-vivo, AD, NA
*antiOx↑, *neuroP↑, *AntiCan↑, *memory↑, *ROS↓, *BDNF↑, *cognitive↑,
3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, TumCP↓, Apoptosis↑, TumMeta↑, ChemoSen↑, BioAv↓, Dose↝, BioAv↓, BioAv↑, SOD↑, Catalase↑, GPx↑, IL2↑, IL4↑, IL1↑, TNF-α↑, GSH↑, GPx↑, GSTA1↑, GSR↑, PPARγ↑, Casp3↑, NF-kB↓, COX2/PTGS2↓, Bcl-2↑, BAX↓, P53↓, CHK1↓, Chk2↓, γH2AX↓, DNAdam↓, ROS↓, P21↑, PCNA↓, β-catenin/ZEB1↓, PGE2↓, ERK↓, cMyc↓, cycE/CCNE↓, JAK1↓, STAT3↓, SIRT1↑, cl‑PARP↑, cycD1/CCND1↓, TNF-α↓, IL6↓, p65↓, MMP2↓, MMP9↓, Wnt↓,
3275- Lyco,    Multifaceted Effects of Lycopene: A Boulevard to the Multitarget-Based Treatment for Cancer
- Review, Var, NA
TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, P21↑, P53↑, GSK‐3β↓, p27/CDKN1B↓, Akt↓, mTOR↓, ROS↓, MMPs↓, TumCI↓, TumCMig↓, NF-kB↓, *iNOS↓, *COX2/PTGS2↓, lipid-P↓, GSH↑, NRF2↑,
3268- Lyco,    Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders
- Review, AD, NA
*BioAv↓, *AntiCan↑, *ROCK1↓, *Ki-67↓, *ICAM-1↓, *cardioP↑, *antiOx↑, *NQO1↑, *HO-1↑, *TNF-α↓, *IL22↓, *NRF2↑, *NF-kB↓, *MDA↓, *Catalase↑, *SOD↑, *GSH↑, *cognitive↑, *tau↓, *hepatoP↑, *MMP2↑, *AST↓, *ALAT↓, *P450↑, *DNAdam↓, *ROS↓, *neuroP↑, *memory↑, *Ca+2↓, *Dose↝, *Dose↑, *Dose↝, *toxicity∅, PGE2↓, CDK2↓, CDK4↓, STAT3↓, NOX↓, NOX4↓, ROS↓, *SREBP1/SREBF1↓, *FASN↓, *ACC↓,

Showing Research Papers: 1 to 50 of 51
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 51

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 2,   antiOx↑, 6,   ARE↑, 1,   Catalase↑, 2,   GPx↑, 2,   GSH↓, 1,   GSH↑, 2,   GSR↑, 1,   GSTs↑, 1,   lipid-P↓, 2,   MDA↑, 1,   NOX↓, 1,   NOX4↓, 1,   NRF2↑, 2,   ROS↓, 15,   ROS↑, 13,   ROS⇅, 3,   i-ROS↓, 1,   mt-ROS↑, 1,   SOD↓, 1,   SOD↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CholSyn↓, 1,   GSK‐3β↓, 1,   p‑GSK‐3β↓, 1,   LDL↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 11,   BAX↓, 1,   BAX↑, 3,   Bax:Bcl2↑, 6,   Bcl-2↓, 3,   Bcl-2↑, 1,   Casp3↑, 5,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   iNOS↓, 1,   p38↓, 1,   survivin↓, 2,   β-TRCP↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2,   p‑Akt↓, 1,   CIP2A↓, 1,   EGFR↓, 1,   ERK↓, 2,   p‑ERK↓, 1,   IGF-1R↓, 1,   JAK1↓, 2,   mTOR↓, 1,   RAS↓, 1,   Sp1/3/4↓, 1,   STAT3↓, 3,  

Transcription & Epigenetics(tgid=7) ⓘ

cMyc↓, 4,   tumCV?, 1,   tumCV↓, 3,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   DNAdam↑, 4,   P53↓, 1,   P53↑, 5,   cl‑PARP↑, 1,   PCNA↓, 1,   γH2AX↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK2↑, 1,   CDK4↓, 2,   CHK1↓, 1,   Chk2↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 8,   cycE/CCNE↓, 3,   cycE/CCNE↑, 1,   P21↑, 4,   p27/CDKN1B↓, 1,   p27/CDKN1B↑, 2,   TumCCA↓, 1,   TumCCA↑, 5,  

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

HMGCR↓, 1,   p‑Jun↓, 1,   TumCG↓, 3,   TumCP↓, 5,   TumCP↑, 1,   Wnt↓, 3,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   APC↑, 1,   E-cadherin↑, 1,   MMP2↓, 3,   MMP7↓, 2,   MMP9↓, 5,   MMPs↓, 1,   Rho↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCA↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumMeta↑, 1,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   MMP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 5,   IL1↑, 1,   IL10↓, 1,   IL12↓, 1,   IL1β↓, 2,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   Inflam↓, 3,   NF-kB↓, 8,   NF-kB↑, 1,   p65↓, 1,   PGE2↓, 4,   TNF-α↓, 3,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 5,   Dose↓, 1,   Dose↑, 2,   Dose↝, 2,   eff↓, 2,   eff↑, 2,   GSTA1↑, 1,   P450↓, 1,   selectivity↑, 2,   Synergy↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,   EGFR↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   cardioP↑, 1,   chemoP↑, 1,   neuroP↑, 1,   Risk↓, 4,  
Total Targets: 141

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 22,   ARE↑, 1,   Catalase↑, 7,   GPx↑, 5,   GSH↑, 6,   GSR↑, 1,   GSTs↓, 1,   GSTs↑, 3,   H2O2↓, 1,   HO-1↑, 6,   lipid-P↓, 4,   MDA↓, 7,   MPO↓, 1,   NOX4↓, 2,   NQO1↑, 3,   Nrf1↑, 1,   NRF2↓, 1,   NRF2↑, 10,   ROS↓, 22,   ROS↑, 1,   ROS⇅, 4,   SOD↑, 8,   TAC↑, 2,   Trx1↑, 1,   VitC↑, 1,   VitE↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 3,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1,   ALAT↓, 2,   CRM↑, 1,   FASN↓, 1,   LDL↓, 2,   SIRT1↑, 1,   SREBP1/SREBF1↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 3,   BAX↓, 1,   Bcl-2↑, 2,   Casp3↓, 2,   Casp9↓, 1,   iNOS↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   Akt↑, 3,   ERK↓, 1,   JNK↓, 1,   MAPK↓, 1,   PI3K↑, 3,   STAT3↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 2,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

Ki-67↓, 2,  

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

Ki-67↓, 2,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   Ca+2↓, 1,   LRP1↑, 1,   MMP2↑, 1,   MMPs↓, 1,   MUC1↑, 1,   ROCK1↓, 1,   TGF-β↓, 1,   TGF-β1↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 3,   VCAM-1↓, 1,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   IBI↑, 1,   MMP↓, 1,   MMP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 6,   ICAM-1↓, 2,   IFN-γ↓, 1,   IL1↓, 3,   IL10↓, 1,   IL10↑, 3,   IL12↓, 1,   IL1β↓, 6,   IL22↓, 1,   IL6↓, 7,   IL8↓, 2,   IL8↑, 1,   Inflam↓, 14,   NeuroI↓, 1,   NF-kB↓, 11,   p65↓, 1,   RAGE↓, 2,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 10,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   Ach↑, 1,   AChE↓, 2,   ADAM10↑, 1,   BDNF↑, 5,   MAOA↓, 2,   NGF↑, 1,  

Protein Aggregation(tgid=19) ⓘ

APP↓, 1,   Aβ↓, 2,   Aβ42↓, 2,   BACE/β-secretase↓, 2,   tau↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 7,   BioAv↝, 5,   ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 5,   eff↑, 1,   Half-Life↑, 2,   P450↑, 1,   Synergy↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 2,   BMD↑, 1,   BP↓, 2,   creat↓, 1,   IL6↓, 7,   LDH↓, 2,   RAGE↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiArt↑, 1,   AntiCan↑, 4,   AntiMyl↑, 1,   cardioP↑, 9,   chemoP↑, 1,   cognitive↑, 6,   hepatoP↑, 2,   Learn↑, 1,   memory↑, 6,   neuroP↑, 11,   Obesity↓, 1,   radioP↑, 1,   RenoP↑, 4,   toxicity∅, 2,   Wound Healing↑, 1,  
Total Targets: 134

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
51 Lycopene
2 Chemotherapy
1 beta-carotene(VitA)
1 5-fluorouracil
1 Cisplatin
1 Resveratrol
1 Vitamin C (Ascorbic Acid)
1 Quercetin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:119  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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