Melatonin Cancer Research Results

MLT, Melatonin: Click to Expand ⟱
Features:
Hormone in the body made by pineal gland.
• Melatonin is a potent antioxidant. It neutralizes reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are involved in DNA damage and cancer progression.
• Melatonin has been shown to modulate apoptotic pathways by influencing mitochondrial permeability, cytochrome c release, and caspase activation.
• In several cancer cell models, melatonin appears to promote apoptosis in malignant cells while sparing normal cells.

The most well-known indolamines are serotonin and melatonin, both of which play significant roles in regulating mood, sleep, and overall mental well-being.

Melatonin doses (20 mg to even 40 mg per day), often given as an adjuvant treatment for cancer.
-The plasma half-life of melatonin is generally in the range of approximately 20 to 60 minutes
-It has been suggested that administering melatonin at the appropriate phase of the circadian cycle may enhance its anti-tumor activity and reduce the side effects of chemotherapy and radiation therapy.

Bio-availability: Oral melatonin has a low and variable bio-availability (often estimated between 3% and 33%), which means that only a fraction of the ingested dose reaches the bloodstream unchanged.

For proOxidant effect might need >10uM, which might be 100mg dose (assuming 10% bio-availability) Might also be required X10 levels?
-It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations.

Interactions:
-Melatonin could potentially add to the blood pressure–lowering properties of antihypertensive drugs.
-Patients using insulin should be monitored for changes in blood glucose levels.
-Melatonin might interact with drugs like warfarin, aspirin, or clopidogrel.(antiplatelet)


Melatonin — N-acetyl-5-methoxytryptamine is an endogenous indoleamine hormone and chronobiotic synthesized principally by the pineal gland during darkness, with substantial extra-pineal and mitochondrial synthesis also reported. It is formally classified as a hormone/chronobiotic with antioxidant, mitochondrial, immunomodulatory and pleiotropic signaling activity. Standard abbreviations are MEL and MLT. In oncology, melatonin is best regarded as an experimental adjunct rather than an established anticancer drug: extensive preclinical evidence supports antiproliferative, pro-apoptotic, metabolic, anti-angiogenic and treatment-sensitizing actions, but human efficacy evidence remains limited and inconsistent. An important mechanistic feature is its context-dependent redox behavior: it generally suppresses oxidative stress in normal tissues while high pharmacologic concentrations can increase mitochondrial ROS in some cancer models.

Primary mechanisms (ranked):

  1. Mitochondrial reprogramming and intrinsic apoptosis: ↑ mitochondrial activity or stress in susceptible cancer cells, ↑ BAX/cytochrome-c/caspase signaling and ↓ BCL-2, while generally protecting mitochondrial function in normal tissue.
  2. PI3K/AKT/mTOR suppression: ↓ PI3K, AKT, mTOR and downstream survival/proliferation signaling in multiple tumor models.
  3. Metabolic reprogramming: ↓ aerobic glycolysis/Warburg phenotype and, in several models, restoration of pyruvate oxidation and mitochondrial oxidative metabolism.
  4. Redox modulation: predominantly antioxidant in normal cells, but ↑ mitochondrial ROS can become a pro-apoptotic mechanism in selected cancer cells at high concentrations.
  5. HIF-1α/VEGF suppression: ↓ hypoxic adaptation, angiogenesis and associated metabolic signaling.
  6. NF-κB and inflammatory signaling suppression: ↓ tumor-promoting inflammatory and survival signaling.
  7. Cell-cycle arrest and growth inhibition: ↓ cyclins/CDKs/Ki-67 with ↑ p21/p27 in model-dependent settings.
  8. Inhibition of migration, EMT and invasion: ↓ MMP2/MMP9, vimentin and metastatic behavior with ↑ epithelial differentiation markers in some models.
  9. MT1/MT2 receptor and circadian signaling: receptor-dependent and chronobiologic effects can influence proliferation, hormone signaling and cellular metabolism.
  10. Chemosensitization and radiosensitization: preclinical evidence supports synergy with several antineoplastic agents while normal-tissue radioprotection/chemoprotection may occur concurrently.

Bioavailability / PK relevance: Oral melatonin has rapid absorption but extensive first-pass metabolism and highly variable systemic exposure. In one controlled human PK study, 10 mg oral melatonin produced a mean Tmax of approximately 41 minutes, an elimination half-life of approximately 54 minutes and median absolute bioavailability of only about 2.5%. Formulation, CYP1A2 metabolism, age, sex and concomitant drugs can materially alter exposure. Prolonged-release formulations extend exposure but do not reproduce the very high concentrations commonly used in mechanistic cancer experiments.

In-vitro vs systemic exposure relevance: This is a major translational limitation. Many anticancer experiments use approximately 0.1–4 mM melatonin; studies demonstrating cancer-selective mitochondrial ROS frequently use 0.5–1 mM or higher. By comparison, 10 mg orally produced a median/mean peak concentration on the order of a few ng/mL, approximately tens of nanomolar. Thus, common 0.5–1 mM in-vitro concentrations can exceed ordinary oral peak plasma exposure by roughly four to five orders of magnitude. Receptor-mediated, circadian and some endocrine effects occur at much lower concentrations, so high-concentration cytotoxic findings should not be assumed to occur after conventional oral supplementation.

Clinical evidence status: RCT / adjunct use, but not established anticancer therapy. Older small randomized studies and meta-analyses suggested improved response, toxicity and survival with approximately 20 mg/day adjunctive melatonin; however, trial quality and geographic concentration limit confidence. More rigorous modern trials have produced mixed results. A randomized chemotherapy trial did not demonstrate a survival benefit, while several studies report improvements in selected treatment-related symptoms or toxicity. A phase III breast-radiotherapy trial using 20 mg/day found no significant improvement in fatigue or other major patient-reported outcomes. Melatonin should therefore be classified as a clinically studied supportive/adjunctive agent with substantial preclinical anticancer evidence, not as proven cancer treatment.

Safety / deployment: Melatonin is marketed in Canada as a licensed natural health product rather than an approved cancer therapy. Common adverse effects include somnolence, headache, dizziness, nausea and gastrointestinal symptoms. Clinically relevant cautions include additive sedation and potential interactions with anticoagulants, antihypertensive agents, anticonvulsants, immunosuppressants, psychotropic/sedative medications and glucose-lowering therapy. Canadian licensed products advise against driving or operating machinery for several hours after dosing and advise medical consultation for significant liver, kidney, cardiovascular, hormonal, seizure or immune disorders.

Melatonin Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis ↑ BAX; ↓ BCL-2; ↑ cytochrome c; ↑ caspase-3/9 ↓ mitochondrial injury; ↓ inappropriate apoptosis Selective apoptotic pressure One of the most reproducible anticancer phenotypes; direction differs importantly between malignant and stressed normal cells.
2 PI3K AKT mTOR signaling ↓ PI3K; ↓ p-AKT; ↓ mTOR; ↓ p70S6K ↔ or homeostatic modulation ↓ survival and proliferation Observed across several tumor systems and implicated in combination effects with targeted drugs and chemotherapy.
3 Warburg metabolism and glycolysis ↓ glycolysis; ↓ ENO1; ↓ lactate; ↑ mitochondrial oxidation (model-dependent) ↑ mitochondrial metabolic efficiency Metabolic reprogramming Melatonin can shift susceptible tumor cells away from aerobic glycolysis toward mitochondrial metabolism.
4 Mitochondrial ROS signaling ↑ ROS (context-dependent; high concentration often required) ↓ ROS; ↑ antioxidant defense Cancer-selective oxidative stress Dual effect is important. Reverse electron transport can generate pro-apoptotic mitochondrial ROS in selected cancer models, whereas antioxidant activity predominates in normal tissues.
5 HIF-1α VEGF hypoxia axis ↓ HIF-1α; ↓ VEGF ↔ or protective regulation ↓ hypoxic adaptation and angiogenesis Closely linked with metabolic reprogramming and PI3K/AKT/mTOR signaling.
6 NF-κB inflammatory signaling ↓ NF-κB; ↓ IL-6; ↓ COX-2 (model-dependent) ↓ excessive inflammation ↓ inflammatory survival signaling Potentially contributes to both antitumor and normal-tissue protective effects.
7 Cell cycle control ↓ cyclin D1; ↓ CDK4; ↓ Ki-67; ↑ p21/p27 ↔ largely preserved ↑ cell-cycle arrest Cytostatic effects vary with tumor type, concentration and exposure duration.
8 Migration EMT and invasion ↓ MMP2; ↓ MMP9; ↓ vimentin; ↑ E-cadherin ↔ ↓ migration and metastasis Predominantly preclinical evidence.
9 MT1 MT2 and circadian signaling ↓ proliferative signaling (context-dependent) ↑ circadian synchronization Chronobiologic growth regulation Physiologically plausible at substantially lower concentrations than direct high-dose cytotoxic mechanisms.
10 Chemosensitization ↑ chemotherapy response (drug-dependent) ↓ chemotherapy-associated injury in some tissues Therapeutic sensitization Reported with cisplatin, gemcitabine, PI3K inhibitors, TKIs and other agents; most mechanistic evidence remains preclinical.
11 Radiosensitization ↑ radiation response (model-dependent) ↓ radiation injury Differential radio-modulation The cancer-versus-normal-tissue differential is biologically attractive but human evidence for improved tumor control is insufficient.
12 Clinical Translation Constraint High-concentration mechanisms may require exposure far above conventional oral plasma levels Generally well tolerated at clinically studied oral doses Limits extrapolation from cell culture Low and variable oral bioavailability, short plasma half-life, heterogeneous tumor biology, uncertain optimal timing and inconsistent clinical trial efficacy are major constraints.

Melatonin Synergies and Combination Treatments

Ranked by clinical relevance, research frequency, mechanistic support and therapeutic potential. Synergy refers to a quantitatively demonstrated interaction only where specified. Increased combined activity alone does not establish pharmacological synergy.

Rank Combination Application Primary Mechanisms Evidence Synergy Assessment Notes / Interpretation
1 Cisplatin + Melatonin Cancer chemotherapy ↑ apoptosis; ↓ PI3K/AKT; mitochondrial modulation; ↓ normal-tissue ROS Preclinical; clinical adjunct evidence Enhanced activity; formal synergy not consistently established Among the most frequently researched combinations. Potential antitumor sensitization alongside nephroprotection and neuroprotection. Not clinically validated as a means of increasing cisplatin efficacy.
2 5-Fluorouracil + Melatonin Colorectal, esophageal and other cancers ↑ apoptosis; ↑ chemotherapy sensitivity; ↓ tumor survival signaling Preclinical; clinical adjunct literature Quantitative synergy reported in esophageal cancer models High research frequency. Particularly relevant to gastrointestinal oncology.
3 Doxorubicin + Melatonin Breast and other cancers ↑ TRPV1-mediated apoptosis; mitochondrial signaling; ↓ cardiotoxic oxidative injury Preclinical; limited clinical combination evidence Enhanced activity; synergy not consistently quantified Potential dual benefit: increased cancer-cell sensitivity and cardiac protection. Some experiments require high melatonin concentrations.
4 Radiotherapy + Melatonin Solid tumors ↑ cancer-cell radiosensitivity; ↓ normal-tissue oxidative injury; cell-cycle and DNA-repair modulation Human RCTs; preclinical Mixed clinical results Several trials investigated 20 mg/day. Radiation-related symptom outcomes are inconsistent, and improved tumor control remains unproven.
5 Paclitaxel / Docetaxel + Melatonin Breast cancer ↑ apoptosis; ↑ p53/BAX; ↓ invasion; ↓ DJ-1 and ID-1 Preclinical Enhanced cytotoxicity Some cell-line experiments reported combination effects at nanomolar concentrations, improving pharmacological plausibility.
6 Temozolomide + Melatonin Glioblastoma ↑ apoptosis; altered mitochondrial metabolism; ↓ survival and resistance signaling Preclinical; limited clinical investigation Promising combined activity Relevant to glioblastoma, but robust evidence for improved human survival is lacking.
7 Albendazole + Melatonin Glioblastoma ↑ apoptosis; ↑ autophagic cell death; ↓ proliferation In-vitro glioma models Confirmed quantitative synergy in several experimental conditions Combination-index studies demonstrated synergy in C6, RG2 and U87 cells. Translational constraints include drug delivery and achievable exposure.
8 Thymoquinone / Black Seed Oil + Melatonin Breast cancer ↑ apoptosis; altered redox signaling; complementary antiproliferative actions Preclinical Confirmed quantitative synergy with isolated thymoquinone Especially interesting as a natural-product combination. Results using purified thymoquinone cannot automatically be extrapolated to black seed oil with variable thymoquinone content.
9 Sorafenib + Melatonin Leukemia and other cancer models ↑ apoptosis; ↓ survival signaling; modulation of kinase pathways Preclinical Confirmed quantitative synergy in leukemia models Potential for enhanced targeted therapy, but dependent on tumor model and concentration.
10 Tamoxifen + Melatonin Hormone-responsive breast cancer ↓ estrogen-associated proliferation; MT1 signaling; circadian modulation Preclinical Enhanced endocrine response in selected models Mechanistically relevant to ER-positive breast cancers. Not an established clinical strategy for overcoming tamoxifen resistance.
11 Gemcitabine + Melatonin Bladder and pancreatic cancer models ↓ glycolysis; ↓ proliferation; ↑ cytotoxicity Preclinical Enhanced activity Metabolic reprogramming may contribute to sensitization, particularly in bladder cancer models.
12 Alpelisib + Melatonin PIK3CA-mutant breast cancer ↓ PI3K/AKT/mTOR; ↓ HIF-1α; ↑ caspase-3 Preclinical Enhanced activity Mechanistically targeted combination with potential relevance to PI3K-driven malignancies.
13 Resveratrol + Melatonin Cancer prevention and experimental oncology Redox modulation; ↑ apoptosis; regulation of proliferation and inflammation Preclinical Combination benefit reported; synergy uncertain Natural-product combination studied experimentally. Bioavailability and high-concentration in-vitro effects limit extrapolation.
14 Vitamin D3 + Melatonin Breast cancer ↓ cell proliferation; hormone-associated growth regulation In-vitro Synergistic growth inhibition reported in specific models Combined treatment strongly inhibited MCF-7 proliferation in an experimental study; clinical anticancer benefit is unproven.
15 Docosahexaenoic Acid + Melatonin Experimental oncology Lipid metabolism; membrane and redox signaling; apoptosis modulation Preclinical Combined activity under investigation Evidence remains insufficient to rank as an established anticancer synergy.
16 Magnesium + Melatonin Sleep quality and circadian support Melatonin-receptor signaling; neuromuscular relaxation; sleep regulation Human combination-formulation studies Additive benefit plausible; specific synergy unproven Commonly marketed combination. Multi-ingredient trials generally cannot isolate a magnesium-melatonin interaction.
17 L-Theanine + Melatonin Sleep onset and sleep quality Relaxation signaling combined with circadian sleep timing Limited combination-specific human evidence Complementary effects; synergy unproven Common sleep-supplement combination, but direct interaction evidence is limited. May increase subjective sedation.
18 Glycine + Melatonin Sleep support Sleep-associated thermoregulation and circadian regulation Indirect human evidence Complementary; synergy unproven Each has independently investigated sleep effects, but evidence for their combination is inadequate.
19 Lemon Balm + Melatonin Insomnia and anxiety-associated sleep disturbance Relaxation and possible GABAergic modulation; circadian signaling Limited combination-specific clinical evidence Potentially additive; unproven Relevant for sleep formulations. Sedation may be increased, and superiority over melatonin alone is uncertain.
20 Clinical Translation Constraint All oncology combinations Exposure, delivery, pharmacodynamic interactions and tumor heterogeneity Major evidence limitation Not applicable Many studies use melatonin concentrations greatly exceeding ordinary oral plasma exposure. Demonstrated cell-culture synergy does not establish clinical efficacy, dosing or safety with chemotherapy.




Alzheimer’s disease relevance: Melatonin has meaningful mechanistic and clinical relevance to Alzheimer’s disease and mild cognitive impairment through restoration of circadian signaling and sleep, mitochondrial protection, antioxidant and anti-inflammatory activity, and preclinical modulation of amyloid-β and tau pathology. Human randomized evidence suggests possible modest improvements in sleep and cognition, particularly with sustained treatment in MCI or mild disease, but effects are inconsistent and melatonin is not an established disease-modifying therapy for AD.

Melatonin Alzheimer’s Disease Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Circadian rhythm and sleep ↑ circadian synchronization; ↑ sleep duration (modest) Sleep and chronobiologic support Best established clinical rationale in dementia and cognitive impairment.
2 Mitochondrial function ↑ mitochondrial efficiency; ↓ mitochondrial dysfunction Neuroprotection Strong preclinical mechanistic evidence.
3 Oxidative stress ↓ ROS; ↑ GSH; ↑ antioxidant enzymes ↓ oxidative neuronal injury Unlike some high-dose cancer models, antioxidant effects dominate in neuronal and normal-tissue contexts.
4 Neuroinflammation ↓ NF-κB; ↓ inflammatory cytokines ↓ chronic neuroinflammation Predominantly mechanistic and preclinical evidence.
5 Amyloid beta pathology ↓ amyloidogenic processes (preclinical) Potential anti-amyloid activity Human disease-modifying evidence is not established.
6 Tau pathology ↓ tau hyperphosphorylation (preclinical) Potential reduction of neurofibrillary pathology Clinical confirmation is lacking.
7 Cognition ↑ MMSE/global cognition (small; clinical) Possible modest cognitive benefit Recent meta-analyses report a signal, especially in MCI and longer-duration treatment, but heterogeneity remains substantial.


Scientific Papers found: Click to Expand⟱
1351- And,  MLT,    Impact of Andrographolide and Melatonin Combinatorial Drug Therapy on Metastatic Colon Cancer Cells and Organoids
- in-vitro, CRC, T84 - in-vitro, CRC, COLO205 - in-vitro, CRC, HT-29 - in-vitro, CRC, DLD1
eff↑, Ki-67↓, Casp3↑, ER Stress↑, ROS↑, BAX↑, XBP-1↑, CHOP/DDIT3↑, eff↑,
5384- AsP,  MLT,    Synergistic Anticancer Effect of Melatonin and Ascorbyl Palmitate Nanoformulation: A Promising Combination for Cancer Therapy
- in-vivo, Var, NA
AntiCan↑, TumCG↓, Apoptosis↑, DNAdam↑, TumCCA↑, IL6↓, STAT3↓, TumCP↓, Ki-67↓, TumCI↓, TumMeta↓, MMP9↓, eff↑, *Catalase↑, *SOD↑, *GSH↑, *MDA↓, *NO↓, *antiOx↑, *hepatoP↑, *RenoP↑,
4818- ASTX,  MLT,    Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, T47D - in-vitro, Nor, MCF10
TumCD↑, DNAdam↑, *antiOx↑, *AntiTum↑, Inflam↓, tumCV↓, Bcl-2↓, Apoptosis↓, selectivity↑, Synergy↑, Dose↓,
5753- CA,  QC,  MLT,    Effects of Caffeic Acid and Quercetin on In Vitro Permeability, Metabolism and In Vivo Pharmacokinetics of Melatonin in Rats: Potential for Herb-Drug Interaction
- in-vivo, Colon, Caco-2
BioAv↑, CYP1A1↓,
134- CUR,  RES,  MLT,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, ROS↑, Trx1↓, TumCG↓, eff↓, TXNIP↑,
8670- MLT,    Antitumor Effects of Melatonin in Luminal and Triple-Negative Breast Cancer Cells: Metabolic Reprogramming, Redox Regulation, and Cellular Dynamics
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
tumCV↓, TumCMig↓, TumCI↓, GAPDH↓, Hif1a↓, citrate↓, ROS↑, lipid-P↑, LDH↓, G6PD↓, MDA?, Catalase↓, GPx↑, GSH↑, *ROS↓,
8676- MLT,    Effect of melatonin on cognitive function in adults with cognitive impairment: a multi-dimensional meta-analysis of randomized trials
- Review, AD, NA
*cognitive↑, *eff↑,
8675- MLT,    Melatonin combined with antineoplastic drugs or natural products for cancer treatment: An update
- Review, Var, NA
ChemoSen↑, TumCP↓, TumCMig↓, CSCs↓, MDR1↓, chemoP?, IL1β↓, IL6↓, IL8↓, TNF-α↓, COX2/PTGS2↓, iNOS↓, Bcl-2↓, Mcl-1↓, IAP1↓, survivin↓, PCNA↓, Ki-67↓, CC(CDKs/cyclins)↓, TumCMig↓, TumCI↓, Fibronectin↓, Vim↓, N-cadherin↓, MMP2↓, MMP9↓, Synergy↑, Synergy↑, OCT4↓, Nanog↓, ERCC1↓, P-gp/ABCB1↓, EMT↓, Synergy↑, ChemoSen↑,
8674- MLT,    Melatonin supplementation for quality of life in older patients with advanced cancer: a randomized controlled trial
- Trial, Var, NA
Dose↝, eff∅,
8673- MLT,    Therapeutic Potential of Melatonin in Gastrointestinal Cancers: Molecular Mechanisms, Preclinical Evidence and Clinical Implications
- Review, GC, NA
ChemoSen↑, TumVol↓, β-catenin/ZEB1↓, Risk↓, radioP↑, Mucositis↓, Dose↝, toxicity↓, BioAv↓, *antiOx↑, *SOD↑, *GPx↑, *Catalase↑, *NRF2↑, Apoptosis↑, Estro↝, Telomerase↓, *ROS↓, angioG↓, Imm↑, TumCCA↑, Glycolysis↓, OXPHOS↑, mTORC1↓, VEGF↓, Hif1a↓, ROS↓, TumAuto↓, HSP70/HSPA5↓, PI3K↓, Akt↓, mTOR↓, BAX↑, Casp↑, Cyt‑c↑, tumCV↓, TumCMig↓, TumCI↓, TumVol↓, TumW↓, P21↑, P53↑, Synergy↑, ER Stress↑, Synergy↑, RadioS↑, eff↑, eff↑, fatigue↓, Sleep↑,
8672- MLT,    Glioblastoma and Melatonin’s Effects: A Narrative Review
- Review, GBM, NA
selectivity↑, *ROS↓, *DNAdam↓, *SOD↑, *Catalase↑, *GPx↑, *Inflam↓, *EGF↓, *HIF-1↓, Pyruv↓, Glycolysis↓, ROS↑, TumCG↓, IL1β↓, ICAM-1↓, VCAM-1↓, NRF2↓, RadioS↑, OS↑, NAD↓, LDHA↓, MCT4↓, pH↝, ChemoSen↑, Synergy↑, TRPV1↓, Pain↓, Synergy↑, Dose↑,
8671- MLT,    Targeting mitochondrial metabolism in renal cell carcinoma with melatonin: Preclinical evidence and clinical perspectives
- Review, RCC, NA
OXPHOS↑, Warburg↓, ROS↑, Akt↓, mTOR↓, NF-kB↓, HIF-1↓, VEGF↓, MAPK↓, TumCG↓, angioG↓, TumCI↓, Apoptosis↑, TumAuto↑, Synergy↑, *toxicity↓,
8678- MLT,    Melatonin in cancer treatment
- Review, Var, NA
fatigue↓, Nausea↓,
8669- MLT,    Melatonin in lung cancer: integrating molecular mechanisms, tumor microenvironment regulation, apoptotic signaling, and therapeutic opportunities
- Review, Lung, NA
Apoptosis↑, ROS↑, Cyt‑c↑, Bcl-2↓, Casp↑, TumCP↓, TumCI↓, angioG↓, Inflam↓, ChemoSen↑, RadioS↑,
8668- MLT,    Safety and Efficacy of Melatonin for Sleep Disorders in Cancer: A Systematic Review and Meta-Analysis of Randomized Clinical Trials
- Review, Var, NA
Sleep↝,
8667- MLT,  Rad,    The protective effects of melatonin on blood cell counts of rectal cancer patients following radio-chemotherapy: a randomized controlled trial
- Trial, CRC, NA
Dose↝, RBC↑,
8666- MLT,    Clinical impact of melatonin on breast cancer patients undergoing chemotherapy; effects on cognition, sleep and depressive symptoms: A randomized, double-blind, placebo-controlled trial
- Trial, BC, NA
other↝, cognitive↑, memory↑, Verbal↑, neuroP↑, BDNF↓, TrkB↓, chemoP↑,
8665- MLT,  Rad,    Efficacy of Melatonin in Alleviating Radiotherapy-Induced Fatigue, Anxiety, and Depression in Breast Cancer Patients: A Randomized, Triple-Blind, Placebo-Controlled Trial
- Trial, BC, NA
Dose↝, fatigue↓, ANXi↓, antiD↑,
8664- MLT,  Rad,    Melatonin Supplementation for Cancer-Related Fatigue in Patients With Early Stage Breast Cancer Receiving Radiotherapy: A Double-Blind Placebo-Controlled Trial
- Trial, BC, NA
fatigue∅,
8686- MLT,  CAP,    Non-thermal plasma-treated melatonin inhibits the biological activity of HCC cells by increasing intracellular ROS levels and reducing RRM2 expression
- in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
Synergy↑, TumCI↓, TumCMig↓, Apoptosis↑, TumCP↓, TumMeta↓, radioP↑, ROS↑, RRM2↓,
8694- MLT,    Melatonin inhibits glycolysis in hepatocellular carcinoma cells by downregulating mitochondrial respiration and mTORC1 activity
- in-vitro, Liver, NA
mitResp↓, ROS↑, mTORC1↓, cMyc↓, Glycolysis↓, HK2↓, LDHA↓,
8693- MLT,    Mitochondrial cytochrome P450 (CYP) 1B1 is responsible for melatonin-induced apoptosis in neural cancer cells
- in-vitro, GBM, U118MG - in-vitro, neuroblastoma, SH-SY5Y
Apoptosis↑, ChemoSen↑, CYP1B1↑,
8692- MLT,    Melatonin as a Radio-Sensitizer in Cancer
- Review, Var, NA
RadioS↑, radioP↑, ROS↑, DNArepair↓, angioG↓, Inflam↓, Apoptosis↑, Telomerase↓, HSP70/HSPA5↑, P53↑, Glycolysis↓, Dose?, OS∅,
8691- MLT,    Melatonin effect on hypoxia inducible factor-1α and clinical response in patients with oral squamous cell carcinoma receiving neoadjuvant chemotherapy: A randomized controlled trial
- Trial, Oral, NA
Hif1a↓, Dose?, eff∅,
8690- MLT,    Melatonin inhibits proliferation, migration, and invasion by inducing ROS-mediated apoptosis via suppression of the PI3K/Akt/mTOR signaling pathway in gallbladder cancer cells
- vitro+vivo, Gall, NOZ
TumCG↓, TumCMig↓, TumCI↓, ROS↑, PI3K↓, Akt↓, mTOR↓, eff↓, TumCG↓, tumCV↓,
8689- MLT,    Role of melatonin in Alzheimer's disease: From preclinical studies to novel melatonin-based therapies
- Review, AD, NA
*neuroP↑, *Aβ↓, *ROS↓, *NeuroI↓, *Apoptosis↓, *mtDam↓, *GSK‐3β↓, *p‑tau↓, *GFAP↓, *TNF-α↓, *IL6↓, *BACE/β-secretase↓, *PSEN1/PS1↓, *NF-kB↓, *TFAM↑, *Nrf1↑, *NRF2↑, *PGC-1α↑, *MMP↑, *GSH↑, *lipid-P↓, *ChAT↑, *TBARS↓, *SOD↑, *Ca+2↓, *AChE↓, *H2O2↓, *MDA↓, *TAC↑, *SOD↑, *Catalase↑, *BDNF↑, *Bcl-2↑, *Ach↑, *memory↑, *Learn↑, *GSK‐3β↓, *SNAP25↑, *PSD95↑, *p‑CREB↑, *GFAP↓, *RELN↑, *SIRT1↑, *TFAM↑, *APP↓, *ER Stress↓, *GRP78/BiP↓, *Sleep↑, *cognitive↑, *Synergy↑, *NeuroI↓,
8688- MLT,    Melatonin induces apoptosis and cell cycle arrest in cervical cancer cells via inhibition of NF-κB pathway
- in-vitro, Cerv, HeLa - in-vitro, Cerv, SiHa
TumCCA↑, NF-kB↓, COX2/PTGS2↓, MMP9↓, Bcl-2↓, BAX↑,
8687- MLT,    Melatonin induces cell cycle arrest and suppresses tumor invasion in urinary bladder urothelial carcinoma
- in-vitro, CRC, T24/HTB-9 - in-vitro, Bladder, UMUC3
TumCP↓, TumCCA↑, Hif1a↓, NF-kB↓, Bcl-2↓, ROS↑, Akt↓, PCNA↓, cycD1/CCND1↓, BAX↓, Apoptosis?, ChemoSen↑, Wnt↓, β-catenin/ZEB1↓, COX2/PTGS2↓, PGE2↓, NF-kB↓, PI3K↓, Akt↓, P53↑, P21↑, *cardioP?, *NRF2↑, *HO-1↑, *RenoP↑, chemoP↑,
8677- MLT,    Evaluating the Cardioprotective Effects of Melatonin in Non-metastatic Breast Cancer Patients Receiving Doxorubicin Plus Cyclophosphamide: A Triple-Blind, Placebo-Controlled Randomized Controlled Trial
- Trial, BC, NA
cardioP↑, *other↑,
8685- MLT,    Melatonin acts synergistically with pazopanib against renal cell carcinoma cells through p38 mitogen-activated protein kinase-mediated mitochondrial and autophagic apoptosis
- vitro+vivo, RCC, 786-O
Synergy↑, Casp↑, LC3II↑, TumAuto↑, Apoptosis↑, MAPK↑, TumCG↓, MMP?, Bax:Bcl2↑,
8684- MLT,    Intratumoral injection of melatonin enhances tumor regression in cell line-derived and patient-derived xenografts of head and neck cancer by increasing mitochondrial oxidative stress
- in-vivo, SCC, CAL27 - in-vivo, Tong, SCC9
TumCP↓, TumCG↓, ROS↑, Apoptosis↑, TumCMig↓, TumMeta↓,
8683- MLT,    Intra-tumor ROS amplification by melatonin interferes in the apoptosis-autophagy-inflammation-EMT collusion in the breast tumor microenvironment
- in-vivo, BC, NA
ROS↑, SIRT1↑, IL6↓, STAT3↓, NF-kB↓, PI3K↓, Akt↓, mTOR↓, TumCP↓, tumCV↓, JNK↑, P53↑, Bax:Bcl2↑, cl‑Casp3↑, Apoptosis↑, eff∅, TumAuto↑, EMT↓, Half-Life↓, CompStab↓, BioAv↓, Dose↝, TumW↓, TumVol↓, Ki-67↓, PTEN↑,
8682- MLT,    Melatonin suppresses tumor proliferation and metastasis by targeting GATA2 in endometrial cancer
- vitro+vivo, EC, NA
GATA2↑, TumCP↓, TumMeta↓,
8681- MLT,    Melatonin changes energy metabolism and reduces oncogenic signaling in ovarian cancer cells
- in-vitro, Ovarian, SKOV3
HIF-1↓, G6PD↓, GAPDH↓, PDH↓, CS↓, PFK1↓, LDH↓, PDH↑, lactateProd↓, glut↓, CREB↓, JNK↓, NF-kB↓, p38↓, ERK↓, Akt↓, P70S6K↓, STAT↓, Warburg↓, GlutaM↓,
8680- MLT,    Function of intramitochondrial melatonin and its association with Warburg metabolism
- Analysis, Var, NA
mt-ROS↓, Glycolysis↓, TumCP↓, SIRT3↑, FOXO↑, PDH↑, Hif1a↓, PDK1 / PDPK1↓, Warburg↓,
8679- MLT,    Targeting Melatonin to Mitochondria Mitigates Castration-Resistant Prostate Cancer by Inducing Pyroptosis
- in-vitro, Pca, NA
Synergy↑, ROS↑, MMP↝, mitResp↓, T-cadherin↓, OXPHOS↓, Glycolysis↓, Pyro↑,
8661- MLT,    Melatonin effect on breast and ovarian cancers by targeting the PI3K/Akt/mTOR pathway
- in-vitro, BC, NA - in-vitro, Ovarian, NA
PTEN↓, PI3K↓, Akt↓, mTOR↓, mTORC1↓, MDM2↓, BAD↑, Bcl-xL↑, P53↓, TumAuto↑, ULK1/ATG1↑, p‑Beclin-1/ATG6↑,
1785- MLT,    Antitumoral melatonin-loaded nanostructured lipid carriers
- in-vitro, Var, NA
selectivity↑, TumCD↑,
971- MLT,    Melatonin down-regulates HIF-1 alpha expression through inhibition of protein translation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
Hif1a↓, VEGF↓, p‑p70S6↓,
995- MLT,    Melatonin Treatment Triggers Metabolic and Intracellular pH Imbalance in Glioblastoma
- vitro+vivo, GBM, NA
LDHA↓, MCT4↓, lactateProd↓, i-pH↓, ROS↑, ATP↓, TumCD↑, TumCCA↑, PDH↓, Glycolysis↓, GlucoseCon↓, TumCG↓,
1042- MLT,    Melatonin Downregulates PD-L1 Expression and Modulates Tumor Immunity in KRAS-Mutant Non-Small Cell Lung Cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H460 - in-vitro, Lung, LLC1
PD-L1↓, YAP/TEAD↓, TAZ↓, TumCG↓,
1063- MLT,    HDAC1 inhibition by melatonin leads to suppression of lung adenocarcinoma cells via induction of oxidative stress and activation of apoptotic pathways
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
AntiCan↑, TumCMig↓, GSH↓, Casp3↑, Apoptosis↑, ROS↑, HDAC1↓, Ac-histone H3↑, PUMA↑, BAX↑, PCNA↓, Bcl-2↓,
1775- MLT,  Chemo,  Rad,    A Systematic Review of the Chemo/Radioprotective Effects of Melatonin against Ototoxic Adverse Effects Induced by Chemotherapy and Radiotherapy
- Review, Var, NA
chemoP↑, radioP↑, antiOx↑, Inflam↑,
1776- MLT,    Therapeutic strategies of melatonin in cancer patients: a systematic review and meta-analysis
- Review, Var, NA
Remission↑, OS↑, neuroP↑, VEGF↓, KISS1↑, TumCP↓, ChemoSideEff↓, radioP↑, Dose∅, *ROS↓, DNArepair↑, ROS↑,
1777- MLT,    Melatonin as an antioxidant: under promises but over delivers
- Review, Var, NA
*ROS↓, *Fenton↓, *antiOx↑, *toxicity∅, *GPx↑, *GSR↑, *GSH↑, *NO↓, *Iron↓, *Copper↓, *IL1β↓, *iNOS↓, *Casp3↓, *BBB↑, *RenoP↑, chemoP↑, *Ca+2↝, eff↑, *PKCδ?, ChemoSen↑, eff↑, Akt↓, DR5↑, selectivity↑, ROS↑, Synergy↑,
1778- MLT,    Melatonin: a well-documented antioxidant with conditional pro-oxidant actions
- Review, Var, NA - Review, AD, NA
*ROS↓, *antiOx↓, ROS↑, selectivity↑, Dose↑, *mitResp↑, *ATP↑, *ROS↓, eff↑, ROS↑, Dose↑, *toxicity∅, ROS↑, eff↓, ROS↝, Dose↑, other↑,
1779- MLT,    Therapeutic Potential of Melatonin Counteracting Chemotherapy-Induced Toxicity in Breast Cancer Patients: A Systematic Review
- Review, BC, NA
QoL↑, OS↑, Dose∅, antiOx↑, ROS↑, SOD↑, Catalase↑, GPx↑, Risk↓, NK cell↑, IL1β↓, IL6↓, TNF-α↓, radioP↑, chemoP↑, TumVol↓, TumMeta↓, angioG↓, ChemoSen↑, eff↑,
1780- MLT,    Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing
- Review, Var, NA
*antiOx↑, *toxicity↓, ChemoSen↑, *eff↑, *mitResp↑, *ATP↑, *ROS↓, *CardioT↓, *GSH↑, *NOS2↓, *lipid-P↓, eff↑, *HO-1↑, *NRF2↑, *NF-kB↑, TumCP↓, eff↑, neuroP↑,
1781- MLT,    Melatonin in patients with cancer receiving chemotherapy: a randomized, double-blind, placebo-controlled trial
- Trial, Lung, NA
QoL↑, OS∅, selectivity↑,
1782- MLT,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumCG↑, TumMeta↑, ChemoSideEff↓, radioP↑, ChemoSen↑, *ROS↓, *SOD↑, *GSH↑, *GPx↑, *Catalase↑, Dose∅, VEGF↓, Synergy↑, Hif1a↓, GLUT1↑, GLUT3↑, CAIX/CA9↑, P21↑, p27/CDKN1B↑, PTEN↑, Warburg↓, PI3K↓, Akt↓, NF-kB↓, cycD1/CCND1↓, CDK4↓, CycB/CCNB1↓, CDK4↓, MAPK↑, IGF-1R↓, STAT3↓, MMP9↓, MMP2↓, MMP13↓, E-cadherin↑, Vim↓, RANKL↓, JNK↑, Bcl-2↓, P53↑, Casp3↑, Casp9↑, BAX↑, DNArepair↑, COX2/PTGS2↓, IL6↓, IL8↓, NO↓, T-Cell↑, NK cell↑, Treg lymp↓, FOXP3↓, CD4+↑, TNF-α↑, Th1 response↑, BioAv↝, RadioS↑, OS↑,

Showing Research Papers: 1 to 50 of 68
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 68

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↓, 2,   Catalase↑, 1,   CoQ10↝, 1,   GPx↑, 3,   GSH↓, 2,   GSH↑, 1,   lipid-P↑, 1,   MDA?, 1,   NRF2↓, 1,   ROS?, 1,   ROS↓, 1,   ROS↑, 26,   ROS↝, 1,   mt-ROS↓, 1,   SOD↓, 1,   SOD↑, 1,   TAC↓, 1,   Trx1↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

compI↑, 1,   compII↑, 1,   CS↓, 1,   ETC↓, 1,   mitResp↓, 2,   mRET↑, 1,   mtDam↑, 1,   OCR↑, 1,   OXPHOS↓, 1,   OXPHOS↑, 4,   PDH↓, 2,   PDH↑, 2,   SIRT3↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATP↓, 1,   ATP↑, 1,   CAIX/CA9↑, 1,   citrate↓, 1,   ENO1↓, 1,   G6PD↓, 2,   GAPDH↓, 2,   GlucoseCon↓, 1,   glut↓, 1,   GlutaM↓, 1,   Glycolysis↓, 10,   HK2↓, 1,   lactateProd↓, 2,   LDHA↓, 3,   MCT4↓, 2,   NAD↓, 1,   PDK1 / PDPK1↓, 1,   PFK1↓, 1,   Pyruv↓, 1,   SIRT1↑, 1,   TCA↑, 1,   Warburg↓, 6,  

Cell Death(tgid=5) ⓘ

Apoptosis?, 1,   Apoptosis↓, 1,   Apoptosis↑, 15,   BAD↑, 1,   BAX↓, 1,   BAX↑, 6,   Bax:Bcl2↑, 3,   Bcl-2↓, 9,   Bcl-xL↑, 1,   BIM↑, 1,   Casp↑, 3,   Casp3↑, 4,   cl‑Casp3↑, 2,   Casp9↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   IAP1↓, 1,   iNOS↓, 1,   Mcl-1↓, 1,   MDM2↓, 1,   p38↓, 1,   PUMA↑, 1,   Pyro↑, 1,   survivin↓, 1,   TumCD↑, 3,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 13,   p‑Akt↓, 2,   CREB↓, 1,   ERK↓, 1,   IGF-1R↓, 1,   JNK↓, 1,   JNK↑, 2,   MAPK↓, 1,   MAPK↑, 2,   mTOR↓, 6,   p‑mTOR↓, 1,   p‑p70S6↓, 1,   P70S6K↓, 1,   p‑P70S6K↓, 1,   PI3K↓, 7,   PTEN↓, 1,   PTEN↑, 2,   STAT↓, 1,   STAT3↓, 3,  

Transcription & Epigenetics(tgid=7) ⓘ

Ac-histone H3↑, 1,   cMyc↓, 1,   FOXO↑, 1,   GATA2↑, 1,   HDAC1↓, 1,   KISS1↑, 1,   OCT4↓, 1,   other↑, 2,   other↝, 1,   tumCV↓, 5,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 2,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p‑Beclin-1/ATG6↑, 1,   LC3II↑, 1,   TumAuto↓, 1,   TumAuto↑, 4,   ULK1/ATG1↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   DNArepair↓, 1,   DNArepair↑, 2,   ERCC1↓, 1,   P53↓, 1,   P53↑, 5,   PCNA↓, 3,   Telomerase↓, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CC(CDKs/cyclins)↓, 1,   CDK4↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   Ki-67↓, 5,   P21↑, 3,   p27/CDKN1B↑, 1,   RRM2↓, 1,   TumCCA↑, 7,  

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

CSCs↓, 1,   Ki-67↓, 5,   mTORC1↓, 3,   Nanog↓, 1,   TAZ↓, 1,   TumCG↓, 11,   TumCG↑, 1,   TumCP↓, 14,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   EMT↓, 3,   Fibronectin↓, 1,   MMP13↓, 1,   MMP2↓, 2,   MMP9↓, 5,   N-cadherin↓, 2,   Snail↓, 1,   T-cadherin↓, 1,   TumCI↓, 8,   TumCMig↓, 8,   TumMeta↓, 6,   TumMeta↑, 1,   TXNIP↑, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 5,   HIF-1↓, 2,   Hif1a↓, 9,   NO↓, 1,   VCAM-1↓, 1,   VEGF↓, 6,   VEGFR1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↑, 1,   GLUT3↑, 1,   MMP?, 1,   MMP↑, 2,   MMP↝, 1,   TRPV1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 4,   FOXP3↓, 1,   ICAM-1↓, 1,   IL1β↓, 3,   IL6↓, 5,   IL8↓, 2,   Imm↑, 1,   Inflam↓, 3,   Inflam↑, 1,   NF-kB↓, 7,   NK cell↑, 2,   PD-L1↓, 1,   PGE2↓, 1,   T-Cell↑, 1,   Th1 response↑, 1,   TNF-α↓, 2,   TNF-α↑, 1,   Treg lymp↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↝, 1,   i-pH↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↓, 1,   TrkB↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Estro↝, 1,   PPARγ↓, 1,   RANKL↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 13,   CompStab↓, 1,   CYP1A1↓, 1,   CYP1B1↑, 1,   Dose?, 3,   Dose↓, 1,   Dose↑, 4,   Dose↝, 6,   Dose∅, 4,   eff↓, 5,   eff↑, 11,   eff∅, 3,   Half-Life↓, 1,   MDR1↓, 1,   P-gp/ABCB1↓, 1,   RadioS↑, 5,   selectivity↑, 6,   Synergy↑, 16,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 5,   LDH↓, 2,   PD-L1↓, 1,   RBC↑, 1,   Verbal↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   antiD↑, 1,   AntiTum↑, 2,   ANXi↓, 1,   cardioP↑, 1,   chemoP?, 1,   chemoP↑, 5,   ChemoSideEff↓, 2,   cognitive↑, 1,   fatigue↓, 3,   fatigue∅, 1,   memory↑, 1,   Mucositis↓, 1,   Nausea↓, 1,   neuroP↑, 3,   OS↑, 5,   OS∅, 2,   Pain↓, 1,   QoL↑, 2,   radioP↑, 8,   Remission↑, 3,   Risk↓, 3,   Sleep↑, 1,   Sleep↝, 1,   toxicity↓, 1,   TumVol↓, 5,   TumW↓, 2,  
Total Targets: 254

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 7,   Catalase↑, 6,   Copper↓, 1,   Fenton↓, 1,   GPx↑, 5,   GSH↑, 5,   GSR↑, 1,   H2O2↓, 1,   HO-1↑, 2,   Iron↓, 1,   lipid-P↓, 2,   MDA↓, 2,   Nrf1↑, 1,   NRF2↑, 4,   ROS↓, 13,   SOD↑, 6,   SOD2↑, 1,   TAC↑, 1,   TBARS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

DRP1/DNM1L↓, 2,   EGF↓, 1,   ETC↑, 1,   FIS1↓, 1,   MFN1↑, 1,   MFN2↑, 1,   mitResp↑, 2,   mtDam↓, 1,   OPA1↑, 1,   OXPHOS↑, 1,   PGC-1α↑, 3,   TFAM↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

mt-ACC⇅, 1,   ATP↑, 3,   FAO↑, 1,   Glycolysis↝, 1,   GSK‐3β↓, 2,   PDKs↑, 1,   PKM1↑, 1,   PKM2↑, 1,   SIRT1↑, 3,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Bcl-2↑, 1,   Casp3↓, 1,   iNOS↓, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

p‑CREB↑, 1,   Hippo↑, 1,   PKCδ?, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,   other↓, 1,   other↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,   GRP78/BiP↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

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

CLOCK↝, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 2,   Ca+2↝, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

HIF-1↓, 1,   NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   MMP↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   NeuroI↓, 2,   NF-kB↓, 1,   NF-kB↑, 1,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

GFAP↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

Ach↑, 1,   AChE↓, 1,   ADAM10↑, 3,   BDNF↑, 1,   ChAT↑, 1,   PSD95↑, 1,   RELN↑, 1,   SNAP25↑, 1,  

Protein Aggregation(tgid=19) ⓘ

APP↓, 1,   Aβ↓, 2,   BACE/β-secretase↓, 1,   PSEN1/PS1↓, 1,   p‑tau↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 3,   eff↑, 2,   eff↝, 1,   Synergy↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,   IL6↓, 1,   NOS2↓, 1,   TC↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiMyl↑, 1,   AntiTum↑, 1,   cardioP?, 1,   cardioP↑, 1,   CardioT↓, 1,   cognitive↑, 4,   hepatoP↑, 1,   Learn↑, 2,   memory↑, 2,   neuroP↑, 6,   QoL↑, 1,   RenoP↑, 3,   Risk↓, 1,   Sleep↑, 4,   Stroke↓, 1,   Tinn↓, 2,   toxicity↓, 3,   toxicity∅, 2,  
Total Targets: 109

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#:122  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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