Lycopene 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)
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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↓, 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">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.


Scientific Papers found: Click to Expand⟱
7153- AL,  Gins,  GI,  VitE,  Lyco  Anticoagulant activity of select dietary supplements
- Review, Nor, NA
*AntiAg↑, Garlic Reduces ADP-induced platelet aggregation; thromboxane reduction; reduces clotting time
other?, Ginseng Inhibits thromboxane function
other?, Ginger Alters thromboxane synthesis; inhibits arachidonic acid-induced platelet activation
other?, Vitamin E Reduces platelet adhesion to endothelial cells; increases bleeding time; prevents platelet aggregation
other?, Lycopene Inhibits platelet aggregation

287- ALA,  HCA,  Lyco,    Metabolic treatment of cancer: intermediate results of a prospective case series
PSA↓, one patient
OS↑,

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↑, beta-carotene is known to have pro-oxidant activity in vitro
*ROS⇅, The present study in Hs68 cells demonstrates that lycopene can be either an antioxidant or a pro-oxidant depending on the oxidants used, and that lycopene and beta-carotene behave similarly under the in vitro oxidative conditions.
*Dose↝, Both the antioxidant and pro-oxidant effects of lycopene tended to be dose-dependent

3987- betaCar,  Lyco,    Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection
- Trial, AD, NA
*Synergy↑, A substantially greater absorption of carotenoids was observed when salads were consumed with full-fat than with reduced-fat salad dressing.

5559- betaCar,  Lyco,  Zeax,  Lut,    Low blood carotenoid status in dementia and mild cognitive impairment: A systematic review and meta-analysis
- Review, AD, NA
*antiOx↑, Given their potent antioxidation properties, carotenoids play a role in delaying and preventing dementia and mild cognitive impairment (MCI).
*cognitive↑,
*Risk↓, Our results indicated that blood carotenoid levels were significantly lower in patients with dementia than in controls, despite high heterogeneity across the studies.
*other↓, Our meta-analysis showed that patients with dementia had lower blood lycopene, α-carotene , β-carotene, lutein , zeaxanthin and β-cryptoxanthin than the controls.

4881- CUR,  SFN,  RES,  EGCG,  Lyco  An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↑, natural Nrf2 activators include curcumin, sulforaphane (SF), kahweol, resveratrol, garlic oganosulfur compounds, zerumbone, epigallocatechin-3-gallate, carnosol, cinnamonyl-based compounds, lycopene, and cafestol
*antiOx↑, these chemopreventive agents can activate the antioxidants, phase II detoxification factors, and transducers, and protect the cells from carcinogenic exposure

7741- isoFl,  Lyco,  SIL,    Randomized, double-blind, placebo-controlled crossover study in men with prostate cancer and rising PSA: effectiveness of a dietary supplement
- Trial, Pca, NA
Dose↝, The supplement consisted of soy, isoflavones, lycopene, silymarin and antioxidants as main ingredients.
PSA↓, This translates into a 2.6 fold increase in the PSA doubling time from 445 to 1150 days for the supplement and placebo periods.

4786- Lyco,    Anti-proliferative and apoptosis-inducing activity of lycopene against three subtypes of human breast cancer cell lines
- in-vitro, BC, MDA-MB-468 - in-vitro, BC, MCF7 - in-vitro, BC, SkBr3
TumCP↓, dose-dependent anti-proliferative activity against these cell lines by arresting the cell cycle at the G0/G1 phase at physiologically achievable concentrations found in human plasma.
TumCCA↑,
cl‑PARP↑, demonstrable cleavage of PARP.
ERK↑, Lycopene induced strong and sustained activation of the ERK1/2, with concomitant cyclin D1 suppression and p21 upregulation in these three cell lines
cycD1/CCND1↓,
P21↓,
p‑Akt↓, lycopene inhibited the phosphorylation of Akt and its downstream molecule mTOR, followed by subsequent upregulation of proapoptotic Bax
mTOR↓,
BAX↑,
AntiCan↑, data indicate that the predominant anticancer activity of lycopene in MDA-MB-468 cells
Risk↓, Lycopene has been shown to reduce the risk of overall breast cancer more prominently than other carotenoids

4797- Lyco,    A mechanistic updated overview on lycopene as potential anticancer agent
- Review, Var, NA
AntiCan↑, The anticancer potential of lycopene has been described by various in vitro cells, animal studies, and some clinical trials.
antiOx↓, anticancer potential of lycopene is mainly due to its powerful singlet-oxygen quencher characteristics, simulation of detoxifying/antioxidant enzymes production,
Apoptosis↑, initiation of apoptosis, inhibition of cell proliferation and cell cycle progression as well as modulations of gap junctional communication, the growth factors, and signal transduction pathways
TumCP↓,
TumCCA↑,
Risk↓, The link between increased lycopene consumption and reducedoccurrence of a variety of cancers has been documented by in vitro cells,animal studies, and some clinical studies.
ROS↓, The antioxidant action of lycopene toward ROS
SOD↑, Lycopene can simulate detoxifying/antioxidant enzyme productionsuch as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and glutathione reductase.
Catalase↑, . By stimulating ARE system, the lycopene can increase detoxifying/antioxidant enzymes production such as SOD, CAT, GST
GSTs↑,
ARE↑, The upregulating of the ARE system by lycopere has been studied in human BEAS-2B, HepG2, and MCF7
NRF2↑, figure 1
cycD1/CCND1↓, figure 2
cycE/CCNE↑,
CDK2↑,
p27/CDKN1B↑,
BAX↑,
Bcl-2↓,
P53↑,
ChemoSen↑, Lycopene has also been declared to have a synergistic effect with drugs used in cancer treatment [16,17,27,32]. Lycopene may contribute to improved anticancer effects of enzalutamide

4796- Lyco,    The Anti-proliferation Effects of Lycopene on Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, Nor, MCF10
TumCG↓, increasing concentrations of lycopene had a significant inhibitory effect only on MCF-7 cells
selectivity↑, The two cell lines responded differently to lycopene treatment,
*BioAv↑, The absorption of lycopene into the mucosal cells requires bile acid micelles that are aided by ingesting meals that include dietary fat
*antiOx↑, Lycopene acts as a powerful antioxidant in protecting cells against oxidative damage and loss of normal cell function
*ROS↓, figure 3
Risk↓, Many of the studies that have been done so far with lycopene have looked at its role in prostate cancer, and one study reports a 35% risk reduction of prostate cancer with 10 weekly servings of tomato
*cardioP↑,

4795- Lyco,    Updates on the Anticancer Profile of Lycopene and its Probable Mechanism against Breast and Gynecological Cancer
- Review, BC, NA
TumCG↓, Experimental studies suggest that lycopene can inhibit tumor growth by regulating various signaling pathways for cell growth, arresting the cell cycle, and inducing cell apoptosis.
TumCCA↑,
Apoptosis↑,
P53↝, Lycopene is reported to combat breast cancer specifically via mechanisms, such as regulation of expression of p53 and Bax, suppression of cyclin D
BAX↝,
cycD1/CCND1↓,
ERK↓, inhibiting the activation of ERK and Akt signaling pathway,
Akt↓,
STAT3↓, and gynecological cancer via various signaling pathways such as STAT3, Nrf2, and NF-κB, down-regulation of ITGB1, ITGA5, FAK, MMP9, and EMT markers, etc.
NRF2↝,
NF-kB↓,
ITGB1↓,
ITGA5↓,
FAK↓,
MMP9↓,
EMT↓,

4794- Lyco,    Anticancer Effect of Lycopene in Gastric Carcinogenesis
- Review, GC, NA
*AntiCan↑, Lycopene from red fruits and vegetables has strong anticancer activity in gastric carcinogenesis.
*ROS↓, As one of the most potent antioxidants, lycopene is effective in decreasing oxidative damage by activating antioxidant enzymes such as GSH, GPx and GST.
*GSH↑,
*GPx↑,
*GSTs↑,
TumCG↓, Lycopene treatment inhibits cancer cell growth and induces apoptosis by suppressing ERK signaling pathway.
Apoptosis↑,
ERK↓,
Bcl-2↓, Lycopene decreases Bcl-2 and increases Bax expression, which induce release of cytochrome C from mitochondria, leading to apoptosis.
BAX↑,
Cyt‑c↑,
TumCCA↑, Lycopene treatment inhibits gastric cancer cell proliferation by increasing cell cycle arrest in G0–G1 phase
*DNAdam↓, Lycopene inhibits H. pylori-induced increases in ROS levels and DNA damage in gastric epithelial cells

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↑, Lycopene is a potent antioxidant exhibiting anticancer effects.
AntiCan↑,
ROS↓, results show that lycopene reduced ROS levels and inhibited Jak1/Stat3 activation, alteration of Wnt/β-catenin multiprotein complex molecules, expression of c-Myc and cyclin E, and cell proliferation in H pylori–infected AGS cells.
JAK1↓,
STAT3↓,
Wnt↓,
β-catenin/ZEB1↓,
cMyc↓,
cycE/CCNE↓,
TumCP↓,
Risk↓, Lycopene might be a potential and promising nutrient for preventing H pylori–associated gastric diseases including gastric cancer.

4792- Lyco,    A Comprehensive Review on the Molecular Mechanism of Lycopene in Cancer Therapy
- Review, Var, NA
*AntiCan↑, The antioxidant profile of lycopene promotes anticancerous properties that reduce cancer prevalence by activating cell signaling pathways and gene expression (involved in cancer cell proliferation).
*antiOx↑,
Inflam↓, Lycopene's anti-inflammatory properties suppresses the tumor growth and development- promoting pathways, such as the PI3K/Akt/mTOR pathway.
Wnt↓, anticancer property of lycopene is also evidenced by its inhibi- tory potential of the Wnt/β-catenin signaling pathway that is involved in cancer cell modulation and propagation.
β-catenin/ZEB1↓,
*ROS↓, Lycopene also suppresses and neutralizes oxidative stress and reactive oxygen species (ROS)-induced DNA damage, preventing gene mutation.
BioAv↑, high-pressure homogenization having 80 MPa pressure and 25°C temperature (Carpentieri et al. 2023),and freeze-dried tomatoes (Tan et al. 2021) have improved the bioavailability and bioaccessibility of lycopene.
ROS↓, ycopene against pancreatic acinar cells was determined, it was found that IL- 6 and NF-kB are suppressed by lycopene (2 or 5 μmol/L) after 2 h of cerulein activation, demonstrating their role in neutralizing ROS
Risk↓, Mia et al. (2023) determined prostate cancer-lowering properties of lycopene among 47,365 individuals.
PGE2↓, Lycopene also exhibited its suppressive effect by reducing PGE2, COX-2, and phosphorylated ERK1/2 protein (Marino et al. 2023).
COX2/PTGS2↓,
p‑ERK↓,
P21↑, lycopene and fish oil supplementation was revealed by the elevated expression of cell cycle inhibitors (p21 CIP1/WAF1 and p27Kip1) as well as by the reduced expression of MMP-7, MMP-9, COX-2, PGE2
MMP7↓,
MMP9↓,
ChemoSen↑, It was observed that lycopene and cisplatin act synergistically to arrest cell growth by enhancing Bax & Nrf2 expression and inactivating Bcl-2 and NF-kB pathways
Synergy↑, lycopene silver nanoparticles (LyAgNP) suppressed the progression of HeLa cells and COLO320DM cells

4791- Lyco,    Investigating into anti-cancer potential of lycopene: Molecular targets
- Review, Var, NA
*antiOx↑, Lycopene, the main pigment of tomatoes, possess the strongest antioxidant activity among carotenoids. Lycopene has unique structure and chemical properties.
TumCP↓, the anticancer of lycopene is also considered to be an important determinant of tumor development including the inhibition of cell proliferation, inhibition of cell cycle progression, induction of apoptosis, inhibition of cell invasion, angiogenesis
TumCCA↓,
Apoptosis↑,
TumCI↓,
angioG↓,
TumMeta↓,
*Risk↓, and may be associated with a decreased risk of different types of cancer.
cycD1/CCND1↓, Several studies suggested lycopene decreased cell cycle related proteins, such as cyclin D1, D3 and E, the cyclin-dependent kinases 2 and 4, bcl-2, while decreased phospho-Akt levels and increased p21, p27, p53 and bax levels and in Bax: Bcl-2 ratio
CycD3↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
Bcl-2↓,
P21↑,
p27/CDKN1B↑,
P53↑,
BAX↑,
selectivity↑, lycopene selectively inhibited cell growth in MCF-7 human breast cancer cells but not in the MCF-10 mammary epithelial cells
MMP↓, When treating LNCaP human prostate cancer cells with lycopene, the decreased mitochondrial function could be observed.
Cyt‑c↑, release of mitochondrial cytochrome c and finally led to apoptosis
Wnt↓, Lycopene could inhibit Wnt-TCF signaling pathway in cancer cells.
Synergy↑, Lycopene could synergistically increase QC anticancer activity and inhibit Wnt-TCF signaling in cancer cells.
PPARγ↑, Lycopene could inhibit the growth of cancer cells by activating the PPARγ – LXRα - ABCA1 pathway and decreasing cellular total cholesterol levels
LDL↓,
Akt↓, Lycopene suppressed Akt activation and non-phosphorylated β-Catenin,
PI3K↓, inhibited the proliferation of colon cancer HT-29 cells, which was associated with suppressing PI3K/Akt/mTOR signaling pathway
mTOR↓,
PDGF↓, Lycopene, however, could inhibit PDGF-BB-induced signaling and cell migration in both human cultured skin fibroblasts and melanoma-derived fibroblasts
NF-kB↓, anticancer properties of lycopene may occur to play its role through the inhibition of the NF-κB signaling pathway
ChemoSen↑, lycopene increased the sensitization of cervical cancer cells to cisplatin via the suppression of NF-κB-mediated inflammatory responses, and the modulation of Nrf2-mediated oxidative stress

4790- Lyco,    Role of Lycopene in the Control of ROS-Mediated Cell Growth: Implications in Cancer Prevention
- Review, Var, NA
*antiOx↑, t has also been suggested that lycopene might act as an antioxidant by repairing vitamin E and vitamin C radicals
*ROS⇅, It is hypothesized that lycopene can behave as an antioxidant at low concentrations and as a prooxidant at high concentrations.
TumCP↓, n vitro study, the treatment of androgen-independent prostate cancer cells (PC-3) with various concentrations of lycopene (20, 40 and 60 μM) showed a significant decrease in cell proliferation
AP-1↓, It has been reported that lycopene is able to inhibit AP-1 signalling in mammary cancer cells
eff↓, prostate cancer cell lines, lycopene alone (at physiological concentrations of 1 μM) was without much effect, but in combination with -tocopherol at 50 μM, it exhibited a synergistic effect

4789- Lyco,    Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
- in-vitro, AD, SH-SY5Y
*antiOx↑, Lycopene is an antioxidant protecting from oxidative stress-induced cell damage
*ROS↓, Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells.
*NF-kB↓,
*neuroP↑, Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration.
*MMP↓, As shown in Figure 3C, amyloid-β increased the ratio of green to red fluorescence in the cells, which reflects a decrease in MMP in amyloid β-stimulated cells
*mtDam↓, Lycopene suppressed decrease in OCR in amyloid-β-stimulated cell, suggesting that lycopene prevents mitochondrial damage induced by amyloid-β in the cells.
*OCR↓, In the present study, lycopene significantly inhibited amyloid-β-induced mitochondrial dysfunction, which was proven by its protective effect in reducing both MMP and OCR.

4788- Lyco,    Lycopene as a potential anticancer agent: Current evidence on synergism, drug delivery systems and epidemiology (Review)
- Review, Var, NA
AntiCan↑, It may be associated with a reduction in the morbidity and mortality of several types of cancer, making it a prom‑ ising anticancer agent
ChemoSen↑, present review summarizes the synergistic effects of lycopene as a dietary supplement with other chemotherapy drugs or nutrients, for the enhancement of anticancer effects or the reduction of side effects from chemotherapy drugs.
chemoP↑,
Dose↝, Shao and Hathcock (20) proposed a 75 mg/day intake as the upper limit of lycopene for supplements, as no adverse effects were reported from continuous administration of 75 mg/day lycopene in a 4‑week clinical study
BioAv↑, Thermal processing of tomato products can cause changes in the structure of lycopene to shift and yield cis‑isomers in the product and this form is more bioavailable
BioAv↑, The presence of fat in food also helps enhance the absorption of lycopene (40) and its absorption is influenced by the amount of ingested fat, and the type and emulsification of dietary fat
BioAv↓, avoid the consumption of lycopene concurrently with high dietary fiber, as several types of dietary fiber (e.g. pectin, guar, alginate, etc.) are associated with lower bioavailability of lycopene
cardioP↑, figure 2
AntiDiabetic↑,
hepatoP↑,
neuroP↑,
MAPK↓, 2 mg/kg; 5 mg/kg Inhibition of MAPK signaling pathway (48) and decreased MMP‑2 and MMP‑9 activities through the activation of NM23‑H1, TIMP‑1 and TIMP‑2 expression.
MMP2↓,
MMP9↓,
TIMP1↑,
TIMP2↑,

4801- Lyco,    Lycopene in the Prevention of Cardiovascular Diseases
- Review, CardioV, NA
*BioAv↝, Taking into account the fact that humans are not able to synthesize lycopene de novo, therefore its supply with food is necessary to take advantage of its pro-health properties.
*cardioP↑, protective effect on cardiovascular diseases
*BioAv↑, It is assumed that thanks to the cis form, lycopene is highly bioavailable in the human diet
*BioAv↑, bioavailability of lycopene as a result of its trans to cis isomerization can be achieved by adding fish oil or olive oil to tomato dishes.
*antiOx↑, Antioxidant Effects of Lycopene
*ROS↓, Lycopene is a highly effective antioxidant that, due to the high reactivity between the long polyene chain and free radicals, enables the elimination of singlet oxygen and the reduction of reactive oxygen species (ROS)
*ARE↑, activating the antioxidant response element (ARE)
*SOD↑, it increases the amount of antioxidant enzymes, which include superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*lipid-P↓, figure 3
*COX2/PTGS2↓, lycopene (in the form of watermelon powder) reduced inflammation by reducing the activity of the pro-inflammatory mediator cyclooxygenase 2 (COX-2),
*Inflam↓, Anti-Inflammatory Mechanism of Lycopene
*IL1β↓, inhibits the synthesis and release of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8, and TNF-α.
*IL6↓,
*IL8↑,
*TNF-α↓,
*NF-kB↓, inhibition of the nuclear factor κB (NF-κB)
*BP↓, 15 or 30 mg of lycopene was associated with a significant reduction in systolic BP

4785- Lyco,    The Protective Anticancer Effect of Natural Lycopene Supercritical CO2 Watermelon Extracts in Adenocarcinoma Lung Cancer Cells
- in-vitro, Lung, A549
ROS↑, we found that Lyc W significantly increased the spontaneous release of ROS
NF-kB↑, We found that Lyc W significantly increased the nuclear expression of NF-kB in comparison to medium (p = 0.0289) and to Lyc G, Lyc T and Lyc S treatments
Apoptosis↑, Lyc W Induces Cell 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↑, Owing to its potent antioxidant properties, lycopene can potentially alleviate enhanced levels of proinflammatory mediators (e.g., proinflammatory cytokines IL-8, -6, and -1, and oxidized phospholipids) and prevent NF-κB activation
*IL8↓,
*IL6↓,
*IL1↓,
*NF-kB↓,
Inflam↓, graphical abstract
cycD1/CCND1↓,
MMP2↓,
MMP9↓,
Bcl-2↓,
NF-kB↓,
*Nrf1↑, normal cells
*antiOx↑,
*BDNF↑,
*neuroP↑,
*cardioP↑,
ROS↑, i) enhanced oxidative stress due to prooxidant activities of lycopene under circumstances of tumor cell
Dose↝, There are no known adverse effects from low (12 mg/day) to very high (150 mg/day) intake of dietary or formulated lycopene in a healthy population

4783- Lyco,    Lycopene suppresses gastric cancer cell growth without affecting normal gastric epithelial cells
- in-vitro, GC, AGS - in-vitro, GC, SGC-7901 - in-vitro, Nor, GES-1
TumCG↓, Lycopene specifically suppressed cell growth monitored by Real-Time Cell Analyzer, induced cell cycle arrest and cell apoptosis detected by flow cytometry, and lowered mitochondrial membrane potentials assessed by JC-1 staining of AGS and SGC-7901 ce
TumCCA↑,
Apoptosis↑,
MMP↓,
selectivity↑, while did not affect those of GES-1 cells.
cycE1↓, Lycopene decreased the high expression levels of CCNE1 and increased the levels of TP53 in AGS and SGC-7901 cells without affecting those in GES-1 cells.
TP53↑,
*antiOx↑, Lycopene has a strong antioxidant property without pro-Vitamin A function

4782- Lyco,    New Insights into Molecular Mechanism behind Anti-Cancer Activities of Lycopene
- Review, Var, NA
AntiCan↑, From an anti-cancer perspective, lycopene is often associated with reduced risk of prostate cancer and people often look for it as a dietary supplement which may help to prevent cancer.
TumCP↓, Lycopene was known to be able to suppress cancerous cell proliferation, migration, invasion and adhesion activity in cell culture studies.
TumCMig↓,
TumCI↓,
TumCA↓,
ROS↓, Such suppression was often observed with changes of cancer-related gene expression and relief of oxidative stress
MMP2↓, In general, lycopene could suppress the expression of MMP-2, MMP-7, MMP-9, Sp1, IGF-1R, VEGF while increasing E-cadherin stabilization, connexin 43, nm23-H1, TIMP-1 and TIMP-2 levels
MMP7↓,
MMP9↓,
VEGF↓,
E-cadherin↑,
TIMP1↑,
TIMP2↑,
BioAv↝, it is recommended to avoid consumption of lycopene concurrently with high dietary fiber intake as several types of dietary fiber were found to be able to reduce the bioavailability of lycopene
*IL12↓, lycopene could suppress proinflammatory cytokines such as IL-12, TNF-α, IL-1, IL-1β, IL-6
*TNF-α↓,
*IL1↓,
*IL1β↓,
*IL6↓,
COX2/PTGS2↓, Sprague Dawley rat model, lycopene treatment after induction by azoxymethane caused suppression of aberrant crypt foci, preneoplastic lesion and biomarkers such as COX-2 and iNOS expression
iNOS↓,
*radioP↑, lycopene before induction of DNA damage via X-irradiation as lycopene treatment after irradiation failed to show such DNA protective effect
NF-kB↓, anti-cancer effect of lycopene was also observed in pancreatic cancer cells (PANC-1 cell line) whereby significant reduction of ROS, NF-κB and anti-apoptotic biomarkers (cIAP1, cIAP2 and survivin) was detected while an increment of caspase-3 and Bax:
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↑, One such useful natural antioxidant that has been widely investigated to suppress chemotherapy induced side effects of drugs such as cisplatin is lycopene
Inflam↓, lycopene was found to significantly suppress inflammatory responses in CC cells by inhibiting pro-inflammatory cytokines expression like cyclooxygenase-2 (COX-2), interleukin 1β (IL-1β), IL-6 and tumor necrosis-α (TNF-α)
COX2/PTGS2↓,
IL1β↓,
IL6↓,
TNF-α↓,
ROS↑, Our results indicated the cells treatment with 60 µg/ml lycopene significantly increased ROS generation
ChemoSen↑, Furthermore, L60 and L120 seemed to enhance 5FU-induced ROS generation
SOD↓, significant increase SOD activity

4780- Lyco,    Potential inhibitory effect of lycopene on prostate cancer
- Review, Pca, NA
TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level

4779- Lyco,    Lycopene Inhibits Reactive Oxygen Species-Mediated NF-κB Signaling and Induces Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, PANC1
ROS↓, The results show that the lycopene decreased intracellular and mitochondrial ROS levels, mitochondrial function (determined by the mitochondrial membrane potential and oxygen consumption rate),
NF-kB↓, NF-κB activity, and expression of NF-κB-dependent survival genes in PANC-1 cells.
tumCV↓, Lycopene reduced cell viability with increases in active caspase-3 and the Bax to Bcl-2 ratio in PANC-1 cells
Casp3↑,
Apoptosis↑, Lycopene Induces Apoptosis in PANC-1 Cells
OCR↓, Lycopene Decreases Intracellular and Mitochondrial ROS Levels and OCR in PANC-1 Cells
MMP↓, Lycopene Decreases MMP in PANC-1 Cells
CIP2A↓, Lycopene Decreases Expression of cIAP1, cIAP2, and Survivin in PANC-1 Cells
survivin↓,
Casp3↑, Thus, lycopene induces caspase-3-dependent apoptosis and increased the Bax to Bcl-2 ratio in PANC-1 cells.
Bax:Bcl2↑,

4778- Lyco,    Lycopene exerts cytotoxic effects by mitochondrial reactive oxygen species–induced apoptosis in glioblastoma multiforme
- in-vitro, GBM, GBM8401
BBB↑, lycopene penetration across the blood-brain barrier and its induction of apoptosis, inhibiting proliferation in GBM8401 and T98G GBM cells
Apoptosis↑,
TumCP↑,
P53↑, lycopene promoted p53 upregulation and suppressed cyclins B and cyclin D, leading to cell cycle arrest through ROS-activated ERK pathways.
CycB/CCNB1↓,
cycD1/CCND1↓,
TumCCA↓,
mt-ROS↑, Lycopene induced Mito-ROS accumulation in GBM cells
TumCG↓, Lycopene inhibits the cell growth of GBM cells

4777- Lyco,    Lycopene Inhibits Activation of Epidermal Growth Factor Receptor and Expression of Cyclooxygenase-2 in Gastric Cancer Cells
- in-vitro, GC, AGS
*antiOx↑, Lycopene is a potent antioxidant carotenoid and is responsible for the red color of fruits and vegetables.
tumCV↓, Lycopene decreased cell viability and increased apoptotic indices (DNA fragmentation, apoptosis inducing factor, cleavage of caspase-3 and caspase-9, Bax/Bcl-2 ratio)
DNAdam↑,
Apoptosis↑,
cl‑Casp3↑,
cl‑Casp9↑,
Bax:Bcl2↑,
ROS↓, Lycopene reduced the level of intracellular and mitochondrial ROS
NF-kB↓, attenuation of the DNA-binding activity of NF-κB p50/p50 and the level of COX-2 gene expression.
COX2/PTGS2↓,
EGFR↓, Lycopene Reduces ROS Levels and Inhibits EGFR/Ras/ERK and p38 MAPK Signaling in AGS Cells
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↑, LYC ameliorated histopathological damage and restored brain derived neurotrophic factor (BDNF) levels in the hippocampus of mice.
*antiOx↑, LYC also significantly elevated antioxidant enzymes activities and reduced levels of inflammatory cytokines in the d-galactose-treated mice serum.
*Inflam↓,
*HO-1↑, LYC treatment activated the mRNA expressions of antioxidant enzymes HO-1 and NQO-1, and downregulated inflammatory cytokines IL-1β and TNF-α
*NQO1↑,
*IL1β↓,
*TNF-α↓,
*ROS↓, LYC attenuated neuronal oxidative damage through activation of Nrf2 signaling
*NRF2↑,
*cognitive↑, LYC could ameliorate oxidative stress induced neuroinflammation and cognitive impairment possibly via mediating Nrf2/NF-κB transcriptional pathway.
*BBB↑, LYC exerts antioxidant and anti-inflammatory effects both in vitro and in vivo and possesses blood brain barrier permeability

8412- Lyco,    Brain-targeted lycopene-loaded microemulsion modulates neuroinflammation, oxidative stress, apoptosis and synaptic plasticity in β-amyloid-induced Alzheimer's disease mice
- in-vivo, AD, NA
*MDA↓, Lycopene-loaded microemulsion LME supplementation dramatically attenuated astrocytosis and microgliosis, decreased malondialdehyde production and rescued antioxidant capacities
*antiOx↑,
*eff↑, Nevertheless, most of these phenomena were not observed for mice treated with LOO, implying that LME showed significantly higher therapeutic efficacy against Aβ injury.

8423- Lyco,  Rad,    Tomato Juice Consumption Could Improve Breast Skin Adverse Effects of Radiotherapy in Breast Cancer Patients
- Trial, BC, NA
Dose↝, Twenty-three patients agreed to drink TJ (160 g/day for six months) after the completion of RT
radioP↑, Long-term consumption of tomato juice increases serum carotenoid concentration and contributes to the recovery of early and late skin adverse events caused by radiotherapy.
8-oxo-dG↓, When the correlation between urinary 8-OHdG value and serum lycopene concentration was verified at End and 3M, a negative correlation was confirmed respectively

8422- Lyco,  Rad,    Dietary and Serum Lycopene Levels in Prostate Cancer Patients Undergoing Intensity-Modulated Radiation Therapy
- Trial, Pca, NA
Weight↑, non-significant weight loss was observed in the control group but not the intervention group participants.
other?, A significant positive correlation between serum lycopene, weight, and body mass index, and a negative correlation between serum lycopene and piror nutritional supplement use was detected.
Dose↝, intervention groups additionally received 4 oz (118 mL), 8 oz (237 mL), or 12 oz (355 mL) of TJ. Each ounce of TJ provided∼2 mg lycopene.
Dose↝, we selected a heat-processed food source (TJ), administered the TJ with crackers that contained 5 g fat, and discontinued use of fiber supplements for the duration of the study
*Half-Life↝, Lycopene reaches maximum serum concentrations within 15–48 h after consumption.
radioP?, implied by no weight loss

8421- Lyco,    Lycopene: Sojourn from kitchen to an effective therapy in Alzheimer's disease
- Review, AD, NA
*neuroP↑, Lycopene has established itself as a promising therapy for AD owing to its neuroprotective activities, including antioxidant, anti-inflammatory, and antiamyloidogenic properties
*antiOx↑,
*Inflam↓,
*AntiMyl↑,
*ROS↓, Lycopene is reported to be the most potent molecule among natural carotenoids in its ability to scavenge free radicals.
*MMP↑, # ROS generation and restored mitochondrial membrane potential
*NGF↑, " secretion of growth factors (NGF, BDNF and VEGF),
*BDNF↑,
*VEGF↑,
*Aβ42↓, lower β-amyloid1-42 levels due to downregulation of β-amyloid precursor protein,
*PI3K↑, activating PI3K/Akt/Nrf2 signaling
*Akt↑,
*NRF2↑,
*lipid-P↓, Lycopene mitigated lipid peroxidation and restored the levels of antioxidant defense as reduced GSH, CAT, and SOD.
*GSH↑,
*Catalase↑,
*SOD↑,
*cognitive↑, lycopene (2.5 and 5 mg/kg for 21 days) has been reported to significantly improve colchicine-induced cognitive dysfunction
*Learn↑, In another study, long-term lycopene administration at higher doses (5 and 10 mg/kg p.o. for 15 days) improved the learning ability and retention of learned memory in scopolamineinduced amnesic mice
*memory↑,
*APP↓, Lycopene suppressed the expression of APP and β-secretase 1, and elevated the expression of A Disintegrin and Metalloprotease 10 (ADAM10), thereby inhibited the β-amyloid accumulatio
*BACE/β-secretase↓,
*ADAM10↑,
*NF-kB↓, Furthermore, neuroprotective effect of lycopene is attributed to modulation of Nrf2 signaling and NF-κB translocation in cell model, thereby ameliorate cognitive impairment
*AChE↓, attenuated elevated MDA, AChE
*MAOA↓, lower MAO activity,
*BioAv↝, bioactivity or bioavailability (1030% of dietary administrated).

8420- Lyco,    Anticancer activity of lycopene in HT-29 colon cancer cell line
- in-vitro, CRC, HT-29
Risk↓, An inverse association between serum lycopene levels and the risk of cancers has been pointed out by many prospective and retrospective epidemiological studies
Dose↝, Lycopene at doses of 10 and 20 μM produced a significant antiproliferative effect on HT-29 cells compared to the control
TumCP↓,
Casp3↑, Lycopene (7.89 μM) significantly elevated cleaved caspase 3 (p < 0.01), BAX, and cleaved PARP, 8-oxo-dG levels
BAX↑,
cl‑PARP↑,
8-oxo-dG↑,
γH2AX↑, The levels of γ-H2AX foci are significantly higher while the levels of cytochrome-c are lower (p < 0.05) in lycopene-treated HT-29 cells.
Cyt‑c↑,

8419- Lyco,    Brain-targeted lycopene-loaded microemulsion modulates neuroinflammation, oxidative stress, apoptosis and synaptic plasticity in β-amyloid-induced Alzheimer’s disease mice
- in-vivo, AD, NA
*neuroP↑, brain-targeted LME could exert neuroprotective function via suppressing a series of cascades triggered by Aβ aggregates, thus ameliorating Aβ neurotoxicity and associated abnormalities.
*Aβ↓,
*MDA↓, LME supplementation dramatically attenuated astrocytosis and microgliosis, decreased malondialdehyde production and rescued antioxidant capacities, normalized apoptotic parameters and alleviated neuronal loss
*Astr↓,
*MGlio↓,
*antiOx↑,

8418- Lyco,  docx,    A phase I study of docetaxel plus synthetic lycopene in metastatic prostate cancer patients
- Trial, Pca, NA
Dose↝, The maximum tolerated dose was identified as 150 mg/day of lycopene in combination with docetaxel/ADT for the treatment of metastatic prostate cancer patients.
BioEnh↑, Lycopene increased the AUCinf and C max of plasma docetaxel by 9.5% and 15.1%, respectively
angioG↓, Mechanistically significant effects were seen on angiogenesis and insulin‐like growth factor 1 signalling by lycopene co‐administration with docetaxel/ADT.
IGF-1↓, These data demonstrated that lycopene treatment produces a dose‐dependent reduction in signalling by IGF‐1 through its receptor.
ChemoSen↑, We have shown that lycopene acts synergistically with docetaxel to reduce the viability of human prostate cancer cells in an insulin‐like growth factor 1 (IGF‐1)‐dependent manner and to enhance the anti‐tumour efficacy of docetaxel in a xenog
BioAv↑, The mean lycopene concentrations in plasma at baseline and after 99 days of treatment were .48 ± .37 and .82 ± .49 µmol/L, respectively (p = .0119), an increase of 93.4% (95% confidence interval 25.7%–97.4%) during treatment
CEC↝, Patients treated with lycopene 150 mg daily had a significant increase in CECs only on day 57, with non‐significant changes on all other days.

8417- Lyco,    Lycopene alleviates age-related cognitive deficit via activating liver-brain fibroblast growth factor-21 signalling
- in-vivo, AD, NA
*cognitive↑, LYC protects against age-related cognitive deficit, partly explained by activating liver-brain FGF21 signalling, hence promoting neurotransmitters release via increasing mitochondrial ATP levels and enhancing synaptic vesicle fusion.
*FGF21↑,
*ATP↑,

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↓, Lycopene (LYC) has demonstrated effectiveness in inhibiting inflammatory and oxidative stress markers and appears to exert a modulatory impact on several physiological pathways, behavioral manifestations, and cognitive symptoms associated with AD in
*ROS↓,
*Dose↝, treated with LYC (5 mg/kg orally) for an additional six weeks, followed by a second MWM test before sacrifice.
*Aβ42↓, reduced the accumulation of amyloid β1-42, proinflammatory mediators [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)], malondialdehyde (MDA), and nitrite levels.
*IL1β↓,
*TNF-α↓,
*MDA↓,
*Ach↑, LYC significantly (p < 0.001) decreased the acetylcholine (ACh) concentration, monoamine oxidase (MAO), creatine kinase (CK), and lactate dehydrogenase (LDH) activites. (ACh direction error in reporting)
*MAOA↓,
*LDH↓,
*AChE↓, LYC significantly (p < 0.001) increased the acetylcholinesterase (AChE) activity,(AChe direction error in reporting)
*NRF2↑, nuclear factor erythroid-2-related factor 2 (Nrf2), serotonin, anti-inflammatory mediators [transforming growth factor beta-1 (TGF-β1) and interleukin-10 (IL-10)] lev
*5HT↑,
*TGF-β1↑,
*IL10↑,
*Ki-67↓, suppression of the immunohistochemical expression of cell cycle-related proteins (Ki67 and proliferating cell nuclear antigen [PCNA]
*PCNA↓,

8415- Lyco,  CUR,    Combination of Lycopene and Curcumin Synergistically Alleviates Testosterone-Propionate-Induced Benign Prostatic Hyperplasia in Sprague Dawley Rats via Modulating Inflammation and Proliferation
- in-vivo, BPH, NA
*Dose↝, Rats were divided into six groups and treated daily with a vehicle, lycopene (12.5 mg/kg), curcumin (2.4 mg/kg), a combination of lycopene and curcumin (12.5 mg/kg + 2.4 mg/kg) or finasteride (5 mg/kg).
*Synergy↑, Combination treatment significantly attenuated prostate hyperplasia, alleviated BPH pathological features and decreased the expression of Ki-67 in rats.
*Ki-67↓,
*testos↓, The upregulation of the expression of testosterone, dihydrotestosterone (DHT), 5α-reductase, estradiol (E2) and prostate-specific antigen (PSA) in BPH rats was significantly blocked by the combination treatment.
*DHT↓,
*PSA↓,
*IL1β↓, (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α were strongly inhibited by the combination treatment.
*IL6↓,
*AKT1↓, main targets for inhibiting BPH are AKT1, TNF, EGFR, STAT3 and PTGS2, which are enriched in pathways in cancer.
*TNF-α↓,
*EGFR↓,
*STAT3↓,
*COX2/PTGS2↓,

8414- Lyco,    Exploring the Therapeutic Potential of Lycopene: Mechanisms, Biological Activities, and Health Benefits
- Review, Var, NA - Review, AD, NA
*ROS↓, regulation of oxidative stress, inflammation
*Inflam↓,
*hepatoP↑, Its role containing nephroprotective, hepatoprotective, cardioprotective, and neuroprotective properties, anti-arthritis, anti-obesity, and wound healing has been documented
*cardioP↑,
*neuroP↑,
*AntiArt↑,
*Obesity↓,
*Wound Healing↑,
*BioAv↑, potential of emerging nanoformulation strategies to improve its bioavailability and therapeutic efficacy in disease management.
*GSTs↑, In TD-challenged rats, hepatic activities and gene expression of glutathione S-transferase (GST), thioredoxin-1 (Txn-1), superoxide dismutase (SOD), and catalase (CAT) were decreased; these changes were mitigated by lycopene.
*Trx1↑,
*SOD↑,
*Catalase↑,
*ALAT↓, 5 mg/kg b.w led to partial, dose-dependent improvements in ALT, LDH, AST, and MDA levels
*LDH↓,
*AST↓,
*MDA↓,
*cognitive↑, Lycopene has also been reported to reduce neuronal damage, inhibit oxidative stress, and improve cognitive function in various experimental models.
*memory↑, chronic lycopene administration caused an improvement in memory retention, reducing neuroinflammation
*NeuroI↓,
*Aβ↓, The lycopene administration was found to reduce Aβ accumulation, increase the LRP1 levels, and reduce the RAGE levels in the cerebrospinal fluid or the choroid plexus.
*LRP1↑,
*RAGE↓,
*NRF2↑, lycopene exerts a protective role against global ischemic brain injury through its activation of the Nrf2/HO-1 signaling pathway and anti-apoptotic properties
*HO-1↑,
tumCV?, lycopene significantly decreases cell viability by increasing the Bax/Bcl-2 ratio and promoting DNA fragmentation.
Bax:Bcl2↑,
DNAdam↑,
Apoptosis↑, lycopene induces apoptosis through suppressing β-catenin-c-myc/cyclin D1 axis and reducing ROS levels.
β-catenin/ZEB1↓,
cMyc↓,
cycD1/CCND1↓,
ROS↓,
TumCCA↑, Lycopene plays a substantial role in inhibition of cancer cell growth by causing cell cycle arrest.
Akt↓, Lycopene treatment suppressed Akt activation as well as non-phosphorylated β-catenin protein level
*Synergy↑, The results showed that even at low concentrations, lycopene and EPA worked synergistically to inhibit cancer cell proliferation.
*MDA↓, important reduction in colon tissue L-MDA and down-regulation of NF-κB, TGF-β1, caspase-3, in addition to a noticeable increase in CAT activity and GSH concentration, and up-regulation of Bcl-2 and IL-10 were detected after lycopene treatment
*NF-kB↓,
*TGF-β↓,
*Casp3↓,
*Catalase↑,
*GSH↑,
*Bcl-2↑,
*IL10↑,
*MUC1↑, It enhances mucin production, contributing to improved mucosal barrier function.
*IBI↑,
*RenoP↑, lycopene as renoprotective was confirmed through different mechanisms
*ChemoSen↑, lycopene enhances the sensitivity of cervical cancer cells to cisplatin by downregulating Bcl-2 expression, upregulating Bax expression and reducing cell viability
*Synergy↑, Curcumin Effect on benign prostatic hyperplasia ° The combination treatment attenuated prostate hyperplasia and alleviated BPH pathological features.
*Synergy↑, lycopene, given together with methotrexate, improved serum urea, creatinine levels, reduced oxidative damage markers, and suggestively reversed structural changes in kidney tissue
*BMD↑, It was noticed that substantial bone density loss was not noticed in women taking the tomato sauce, whereas the control group had bone loss.

8413- Lyco,  VitE,    Dietary Lycopene Supplementation Improves Cognitive Performances in Tau Transgenic Mice Expressing P301L Mutation via Inhibiting Oxidative Stress and Tau Hyperphosphorylation
- in-vivo, AD, NA
*memory↑, Supplementations of lycopene or lycopene/vitamin E could significantly ameliorate the memory deficits, observably decreased MDA concentrations and increased GSH-Px activities, and markedly attenuated tau hyperphosphorylation at multiple AD-related si
*MDA↓,
*GPx↑,
*tau↓,
*Synergy↑, Our findings indicated that the combination of lycopene and vitamin E antioxidants acted in a synergistic fashion to bring significant effects against oxidative stress in tauopathies.

4798- Lyco,    Enhancing Anticancer Treatment Efficacy With Lycopene: A Comprehensive Review of Clinical and Preclinical Evidence
- Review, Var, NA
AntiCan↑, Beyond its direct anticancer effects, LYP has been shown to enhance the efficacy of various anticancer agents when used in combination.
ChemoSen↑,
eff↑, LYP, when used in combination with other therapeutic agents, can modulate several key oncogenic signaling pathways, including JAK2, MAPK, Akt/mTOR, IGF-1R, Akt/EZH2/AR, and PPARγ/LXRα/ABCA1.
Synergy↑, alterations have been observed when LYP is combined with various anticancer therapeutics, including radiation therapy, photodynamic therapy, standard chemotherapeutic agents such as cisplatin, 5-fluorouracil, taxanes, and sorafenib

8411- Lyco,    Lycopene destabilizes preformed Aβ fibrils: Mechanistic insights from all-atom molecular dynamics simulation
- Study, AD, NA
*antiOx↑, The highest antioxidant potential and ability to cross blood brain barrier makes lycopene a preferred choice as drug lead for treating AD.
*BBB↑,
*Aβ↓, Lycopene is also observed to destabilize the other polymorphic form of Aβ fibril (2BEG), by accessing the fibrillar cavity and lowering the β-sheet content.

8410- Lyco,    Dietary intake of tomato and lycopene, blood levels of lycopene, and risk of total and specific cancers in adults: a systematic review and dose-response meta-analysis of prospective cohort studies
- Review, Var, NA
Risk↓, High intakes and high levels of lycopene compared to low amounts were, respectively, associated with 5% (Pooled RR: 0.95, 95% CI: 0.92–0.98, I2 = 26.4%, p = 0.002) and 11% (Pooled RR: 0.89, 95% CI: 0.84–0.95, I2 = 15.0%, p < 0.001) re
Dose↝, each 10 μg/dL increase in blood levels of lycopene was associated with a 5% lower risk of overall cancer.
Risk↓, Moreover, we found a linear inverse association between dietary lycopene intake and prostate cancer risk
OS↑, Our findings show that dietary intake and blood levels of lycopene are associated with a lower risk of cancer and death due to cancer.

8409- Lyco,    Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy
- Trial, Pca, NA
Risk↓, An inverse association has been observed between dietary intake of lycopene and the risk of prostate cancer
PSA↓, Plasma prostate-specific antigen levels decreased by 18% in the intervention group, whereas they increased by 14% in the control group
TumCG↓, lycopene supplementation may decrease the growth of prostate cancer. However, no firm conclusions can be drawn at this time because of the small sample size.

8408- Lyco,    Enhanced bioavailability of lycopene when consumed as cis-isomers from tangerine compared to red tomato juice, a randomized, cross-over clinical trial
- Trial, Nor, NA
*BioAv↑, With tangerine tomato juice we observed a marked 8.5-fold increase in lycopene bioavailability compared to red tomato juice (P<0.001). Fractional absorption was 47.70 ± 8.81% from tangerine and 4.98 ± 1.92% from red tomato juices.
*Dose↝, 10 mg lycopene from tangerine (94% cis) or red tomato juice (10% cis)

8407- Lyco,    Lycopene induces cell growth inhibition by altering mevalonate pathway and Ras signaling in cancer cell lines
- in-vitro, Pca, LNCaP
CholSyn↓, lycopene treatment (2.5-10 μM) dose dependently reduced intracellular total cholesterol by decreasing 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase expression and by inactivating Ras
HMGCR↓,
RAS↓,
NF-kB↓, lycopene reduced the Ras-dependent activation of nuclear factor-kappaB (NF-κB)
ROS↓, ycopene significantly reduced ROS production in a dose-dependent manner, starting the inhibition at the concentration of 2.5 uM
p‑Jun↓, Such a reduction was parallel to an inhibition of reactive oxygen species production and to a decrease in the phosphorylation ofc-jun N-terminal kinase, extracellular signal-regulated kinase 1/2 and p38.
TumCCA↑, These effects were also accompanied by an arrest of cell cycle progression and by apoptosis induction
Apoptosis↑,
cycD1/CCND1↓, as evidenced by a decrease in cyclin D1 and phospho-AKT levels and by an increase in p21, p27 and p53 levels and in Bax:Bcl-2 ratio.
p‑Akt↓,
P21↑,
p27/CDKN1B↑,
P53↑,
Bax:Bcl2↑,

7742- Lyco,  isoFl,    Lycopene and soy isoflavones in the treatment of prostate cancer
- Trial, Pca, NA
Risk↓, Dietary intake of lycopene and soy has been associated with a lower risk of prostate cancer
PSA↓, In a previous Phase II clinical trial in prostate cancer patients, we observed prostate-specific antigen (PSA) stabilization with soy isoflavone intake
Dose↝, randomly assigned to receive a tomato extract capsule containing 15 mg of lycopene alone (n = 38) or together with a capsule containing 40 mg of a soy isoflavone mixture (n = 33) twice daily orally for a maximum of 6 mo.
eff↝, However, 35 of 37 (95%) evaluable patients in the lycopene group and 22 of 33 (67%) evaluable patients in the lycopene plus soy isoflavone group achieved stable disease described as stabilization in serum PSA level.

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↓, The decreased cell viability with depleted GSH and increased MDA levels were observed when treated with COL products than control, LYC and AOL
GSH↓,
MDA↑,
ROS↑, In addition, COL products increased ROS levels and percent apoptosis.
Apoptosis↑,

4802- Lyco,    Dietary intake of tomato and lycopene, blood levels of lycopene, and risk of total and specific cancers in adults: a systematic review and dose–response meta-analysis of prospective cohort studies
- Review, Var, NA
Risk↓, In this systematic review and meta-analysis, we found that higher levels of dietary and blood lycopene were, respectively, associated with 5 and 11% lower risk of overall cancer. I


Showing Research Papers: 1 to 50 of 102
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 102

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 2,   antiOx↑, 8,   ARE↑, 1,   Catalase↑, 3,   GPx↑, 4,   GSH↓, 1,   GSH↑, 3,   GSR↑, 1,   GSTs↑, 1,   HO-1↑, 1,   Keap1↝, 1,   lipid-P↓, 2,   MDA↓, 1,   MDA↑, 1,   MPO↓, 1,   NOX↓, 1,   NOX4↓, 1,   NRF2↓, 1,   NRF2↑, 3,   NRF2↝, 2,   ROS↓, 15,   ROS↑, 13,   ROS⇅, 3,   i-ROS↓, 1,   mt-ROS↑, 1,   SOD↓, 1,   SOD↑, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CholSyn↓, 1,   G6PD↓, 1,   Glycolysis↓, 1,   GSK‐3β↓, 1,   p‑GSK‐3β↓, 1,   LDL↓, 2,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 16,   BAX↓, 1,   BAX↑, 7,   BAX↝, 1,   Bax:Bcl2↑, 6,   Bcl-2↓, 5,   Bcl-2↑, 1,   Casp3↑, 7,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 3,   iNOS↓, 2,   p38↓, 1,   survivin↓, 2,   β-TRCP↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 6,   Akt↝, 1,   p‑Akt↓, 3,   Akt2↓, 1,   CIP2A↓, 1,   EGFR↓, 1,   ERK↓, 3,   ERK↑, 1,   p‑ERK↓, 1,   IGF-1R↓, 1,   JAK1↓, 2,   JNK↓, 1,   MAPK↓, 3,   mTOR↓, 4,   mTOR↝, 1,   p‑mTOR↓, 1,   PI3K↓, 2,   PI3K↝, 1,   p‑PI3K↓, 1,   RAS↓, 1,   Sp1/3/4↓, 1,   STAT3↓, 5,  

Transcription & Epigenetics(tgid=7) ⓘ

cMyc↓, 4,   EZH2↓, 1,   FOXO3↓, 1,   other?, 5,   tumCV?, 1,   tumCV↓, 3,  

DNA Damage & Repair(tgid=10) ⓘ

8-oxo-dG↓, 1,   8-oxo-dG↑, 1,   DNAdam↓, 2,   DNAdam↑, 4,   P53↓, 2,   P53↑, 6,   P53↝, 1,   cl‑PARP↑, 3,   PCNA↓, 3,   TP53↑, 1,   γH2AX↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 4,   CDK2↑, 1,   CDK4↓, 4,   CHK1↓, 1,   Chk2↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 13,   CycD3↓, 1,   cycE/CCNE↓, 4,   cycE/CCNE↑, 1,   cycE1↓, 1,   Ki-67↓, 1,   P21↓, 1,   P21↑, 7,   p27/CDKN1B↓, 1,   p27/CDKN1B↑, 4,   TumCCA↓, 2,   TumCCA↑, 11,  

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

HMGCR↓, 1,   IGF-1↓, 2,   p‑Jun↓, 1,   Ki-67↓, 1,   TumCG↓, 7,   TumCP↓, 11,   TumCP↑, 1,   Wnt↓, 4,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   APC↑, 1,   E-cadherin↓, 1,   E-cadherin↑, 1,   EMT↓, 3,   FAK↓, 2,   ITGA5↓, 2,   ITGB1↓, 2,   MMP2↓, 4,   MMP7↓, 3,   MMP9↓, 10,   MMPs↓, 1,   N-cadherin↓, 1,   PDGF↓, 1,   Rho↓, 1,   TIMP1↑, 2,   TIMP2↑, 2,   TumCA↓, 1,   TumCI↓, 5,   TumCMig↓, 3,   TumMeta↓, 1,   TumMeta↑, 1,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

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

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   MMP↓, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 7,   IFN-γ↑, 1,   IL1↑, 2,   IL10↓, 2,   IL10↑, 1,   IL12↓, 1,   IL1β↓, 3,   IL2↑, 1,   IL4↓, 1,   IL4↑, 2,   IL6↓, 4,   Inflam↓, 4,   NF-kB↓, 13,   NF-kB↑, 1,   NF-kB↝, 1,   p65↓, 1,   PGE2↓, 6,   PSA↓, 6,   PSA∅, 1,   TNF-α↓, 5,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

GR↑, 1,   PPARγ↓, 1,   PPARγ↑, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3,   BioAv↑, 5,   BioAv↝, 1,   BioEnh↑, 1,   ChemoSen↓, 1,   ChemoSen↑, 11,   Dose↓, 1,   Dose↑, 2,   Dose↝, 11,   eff?, 1,   eff↓, 2,   eff↑, 5,   eff↝, 1,   GSTA1↑, 1,   P450↓, 1,   RadioS↓, 1,   selectivity↑, 4,   Synergy↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,   CA125↓, 1,   CEC↝, 1,   EGFR↓, 1,   EZH2↓, 1,   IL6↓, 4,   PSA↓, 6,   PSA∅, 1,   TP53↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 8,   AntiDiabetic↑, 1,   cardioP↑, 4,   chemoP↑, 3,   hepatoP↑, 1,   neuroP↑, 2,   OS↑, 3,   QoL↑, 1,   radioP?, 1,   radioP↑, 1,   RenoP↑, 1,   Risk↓, 12,   TumVol↓, 1,   TumW↓, 1,   Weight↑, 1,  
Total Targets: 214

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 34,   ARE↑, 1,   Catalase↑, 7,   Catalase↝, 1,   GPx↑, 6,   GPx↝, 1,   GSH↑, 7,   GSH/GSSG↓, 1,   GSR↑, 1,   GSTs↓, 1,   GSTs↑, 3,   H2O2↓, 1,   HO-1↑, 6,   Keap1↓, 1,   lipid-P↓, 5,   MDA↓, 10,   MPO↓, 1,   NOX4↓, 2,   NQO1↑, 3,   Nrf1↑, 1,   NRF2↓, 1,   NRF2↑, 13,   ROS↓, 22,   ROS↑, 1,   ROS⇅, 4,   SOD↑, 8,   SOD↝, 1,   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,   AMPK↑, 1,   ATP↑, 1,   CRM↑, 1,   FASN↓, 1,   LDL↓, 2,   SIRT1↑, 1,   SREBP1/SREBF1↓, 1,  

Cell Death(tgid=5) ⓘ

APAF1↓, 1,   Apoptosis↓, 4,   BAX↓, 2,   Bcl-2↑, 3,   Casp3↓, 2,   cl‑Casp3↓, 1,   Casp9↓, 1,   cl‑Casp9↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,   p38↓, 2,   Pyro↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2,   Akt↑, 3,   AKT1↓, 1,   EGFR↓, 1,   ERK↓, 1,   JNK↓, 2,   MAPK↓, 2,   mTOR↓, 1,   PI3K↑, 3,   STAT3↓, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 2,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

Ki-67↓, 3,  

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

Ki-67↓, 3,  

Migration(tgid=13) ⓘ

AntiAg↑, 4,   Ca+2↓, 1,   Ca+2↝, 1,   LRP1↑, 1,   MMP2↓, 1,   MMP2↑, 1,   MMPs↓, 1,   MUC1↑, 1,   Rac1↑, 1,   ROCK1↓, 1,   TGF-β↓, 1,   TGF-β1↑, 2,   TIMP2↑, 1,   uPA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   NO↓, 3,   VCAM-1↓, 1,   VEGF↓, 1,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,   IBI↑, 1,   MMP↓, 1,   MMP↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 7,   ICAM-1↓, 2,   IFN-γ↓, 1,   IL1↓, 4,   IL10↓, 1,   IL10↑, 3,   IL12↓, 1,   IL1β↓, 7,   IL22↓, 1,   IL6↓, 9,   IL8↓, 3,   IL8↑, 1,   Inflam↓, 16,   NeuroI↓, 1,   NF-kB↓, 12,   NLRP3↓, 1,   p65↓, 1,   PSA↓, 1,   RAGE↓, 2,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 12,  

Cellular Microenvironment(tgid=17) ⓘ

Astr↓, 1,   MGlio↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   Ach↑, 1,   AChE↓, 2,   ADAM10↑, 1,   BDNF↑, 7,   MAOA↓, 2,   NGF↑, 1,   PSD95↑, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

APP↓, 1,   Aβ↓, 4,   Aβ42↓, 2,   BACE/β-secretase↓, 2,   tau↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

DHT↓, 1,   FGF21↑, 1,   GR↝, 1,   testos↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 8,   BioAv↝, 5,   ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 7,   eff↑, 3,   Half-Life↑, 2,   Half-Life↝, 1,   P450↑, 1,   Synergy↑, 9,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 2,   BMD↑, 1,   BP↓, 2,   creat↓, 1,   EGFR↓, 1,   IL6↓, 9,   LDH↓, 2,   PSA↓, 1,   RAGE↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiArt↑, 1,   AntiCan↑, 5,   AntiMyl↑, 1,   cardioP↑, 9,   chemoP↑, 1,   cognitive↑, 8,   hepatoP↑, 2,   Learn↑, 1,   memory↑, 7,   neuroP↑, 13,   Obesity↓, 1,   radioP↑, 2,   RenoP↑, 4,   Risk↓, 3,   toxicity∅, 2,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,  
Total Targets: 174

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#:%  State#:%  Dir#:%
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