Lycopene / RenoP 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↓, 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.


RenoP, K,Renoprotection/Nephroprotective: Click to Expand ⟱
Source:
Type:
Protects kidneys
-Same as nephroprotective
Opposite is : Nephrotoxicity is toxicity in the kidneys
Scientific Papers found: Click to Expand⟱
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.

3264- Lyco,    Pharmacological potentials of lycopene against aging and aging‐related disorders: A review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.

1713- Lyco,    Lycopene: A Potent Antioxidant with Multiple Health Benefits
- Review, Nor, NA
*antiOx↑, As one of the most potent antioxidants, its capacity to neutralise singlet oxygen is double that of ?-carotene, ten times greater than that of ?-tocopherol, and one hundred and twenty-five times more effective than glutathione
*ROS⇅, lycopene acts as an antioxidant in systems that produce singlet oxygen but behaves as a pro-oxidant in systems that create peroxide
*Dose↝, In low doses, it acts as an antioxidant, but at high doses, it acts as a pro-oxidant
*eff↑, In situation where there is an imbalance between antioxidant defences and ROS production, such as during inflammation or exposure to environmental toxins [91], lycopene may switch from its antioxidant role to a pro-oxidant role
*LDL↓, Wistar rats given a high-fat diet and 50mg/kg body weight of lycopene daily for 3mths had significant reductions in plasma total cholesterol, triglycerides, and lLDL levels but increased HDL cholesterol
*RenoP↑, shown to protect the kidney against chemically induced damage
*Inflam↓, evidence is plentiful demonstrating the anti-inflammatory effects of lycopene both in vitro and in vivo
neuroP↑, mice with Alzheimer's disease induced by ? amyloid, lycopene reduced oxidative stress, decreased neuronal loss, improved synaptic plasticity, and inhibited neuroinflammation
Rho↓, lycopene treatment was demonstrated to have the potential to mitigate vascular arteriosclerosis in allograft transplantation by inhibiting Rho-associated kinases

3531- Lyco,    Lycopene attenuates the inflammation and apoptosis in aristolochic acid nephropathy by targeting the Nrf2 antioxidant system
- in-vivo, Nor, NA
*NRF2↑, After LYC intervened in the body, it activated Nrf2 nuclear translocation and its downstream HO-1 and NQO1 antioxidant signaling pathways
*HO-1↑, Lycopene activates Nrf2-HO-1 antioxidant pathway to inhibit oxidative stress injury induced by AAI exposure in NRK52E cells
*NQO1↑,
*ROS↓, LYC inhibited ROS production by renal tubular epithelial cells, and alleviated mitochondrial damage.
*mtDam↓,
*Bcl-2↑, LYC was able to up-regulate the expression of Bcl-2, down-regulate Bax expression and inhibit the activation of cleaved forms of Caspase-9 and Caspase-3, which finally attenuated the apoptosis
*BAX↓,
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*RenoP↑, Interestingly, there was a significant improvement in damaged renal tissue in mice with AAN after lycopene intervention
*lipid-P↓, lycopene significantly decreased the expression of AAI-induced lipid peroxidation product (MDA), and increased the expression of antioxidant enzyme systems (T-AOC, SOD, and GSH-PX)
*SOD↑,
*GPx↑,
*Inflam↓, Lycopene improves inflammatory responses in the kidneys of AAN mice
*TNF-α↓, TNF-α, IL-6, IL-10, was increased and the expression of IL-12 was decreased in the kidneys of model mice compared with the control group. However, LYC intervention reversed the expression of these genes in a dose-dependent manner
*IL6↓,
*IL10↓,

3281- Lyco,  Chemo,    Lycopene Supplementation for Patients Under Cancer Therapy: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
- Review, Var, NA
eff↑, Our study shows that lycopene supplementation does not modify the main hallmarks of cancer, but it increases circulating lycopene concentration in patients under cancer therapy, which could have a positive impact on potential clinical and molecular o
cardioP↑, A systematic review and meta-analysis reported that tomato and lycopene supplementation have positive effects on cardiovascular risk factors
eff?, lycopene supplementation may have benefits in the oncology population during cancer treatment.
PSA↓, Lycopene supplementation improved PSA levels in patients with an intermediate risk of cancer
RenoP↑, Surprisingly, lycopene has been shown to improve renal makers of nephrotoxicity after cisplatin treatment


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Bax:Bcl2↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cMyc↓, 1,   tumCV?, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Migration(tgid=13) ⓘ

Rho↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

PGE2↓, 1,   PSA↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff?, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 3,   GPx↑, 1,   GSH↑, 2,   GSTs↑, 2,   HO-1↑, 3,   lipid-P↓, 2,   MDA↓, 3,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 3,   ROS↓, 3,   ROS⇅, 1,   SOD↑, 3,   TAC↑, 1,   Trx1↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   CRM↑, 1,   LDL↓, 1,  

Cell Death(tgid=5) ⓘ

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

Kinase & Signal Transduction(tgid=6) ⓘ

ERK↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

LRP1↑, 1,   MUC1↑, 1,   TGF-β↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,   VCAM-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ICAM-1↓, 1,   IL1↓, 1,   IL10↓, 1,   IL10↑, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 4,   NeuroI↓, 1,   NF-kB↓, 2,   RAGE↓, 1,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,   Synergy↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiArt↑, 1,   cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,   Obesity↓, 1,   RenoP↑, 4,   Wound Healing↑, 1,  
Total Targets: 71

Scientific Paper Hit Count for: RenoP, K,Renoprotection/Nephroprotective
5 Lycopene
1 Chemotherapy
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#:1175  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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