Database Query Results : Melatonin, ,

MEL, 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)
Scientific Papers found: Click to Expand⟱
1351- And,  MEL,    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↑, dual therapy significantly promotes CRC cell death
Ki-67↓,
Casp3↑,
ER Stress↑,
ROS↑,
BAX↑,
XBP-1↑,
CHOP↑, Apoptosis signaling molecules BAX, XBP-1, and CHOP were significantly increased
eff↑, combinatorial treatment increased reactive oxygen species (ROS) levels

4818- ASTX,  MEL,    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↑, Astaxanthin increases the melatonin-induced cell death in breast cancer cells
DNAdam↑, Astaxanthin-melatonin combination and DNA damages in breast cancer cells
*antiOx↑, strong anti-oxidative, anti-tumoral, and anti-inflammatory effects.
*AntiTum↑,
Inflam↓,
tumCV↓, Astaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D.
Bcl-2↓,
Apoptosis↓,
selectivity↑, Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D.
eff↑, Furthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.
Dose↓, The results showed that very low doses of astaxanthin reduced survival rate, induced apoptosis, reduced the expression of Bcl2 proteins, and destroyed the DNA in cancerous cells

134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑,
ROS↑,
Trx1↓,

1779- MEL,    Therapeutic Potential of Melatonin Counteracting Chemotherapy-Induced Toxicity in Breast Cancer Patients: A Systematic Review
- Review, BC, NA
QoL↑, melatonin combined with standard chemotherapy lines would derive, at least, a better quality of life for breast cancer patients
OS↑, Moreover, regular doses of 20 mg/day seemed to increase partial response and 1-year survival rates.
Dose∅, regular doses of 20 mg/day
antiOx↑, melatonin possesses antioxidant properties, which may help to protect cells from damage caused by free radicals
ROS↑, elimination of free radicals non-enzymatically transforms melatonin into metabolites with greater antioxidant capacity, which enabling the removal of 10 reactive species per molecule
SOD↑, melatonin upregulates various antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase
Catalase↑,
GPx↑,
Risk↓, individuals with higher melatonin levels show a lower risk of developing breast cancer, and melatonin supplementation may help inhibit the growth and spread of breast cancer cells
NK cell↑, enhance natural killer cell activity
IL1β↓, inhibit the production of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α)
IL6↓,
TNF-α↓,
radioP↑, protect hematopoietic progenitor cells from radiation therapy and chemotherapy
chemoP↑,
TumVol↓, most frequent observations was the ability of melatonin to reduce tumor size
TumMeta↓, decrease the risk of metastasis
angioG↓,
ChemoSen↑, melatonin can synergistically potentiate drug cytotoxicity.
eff↑, 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

4705- MEL,    Melatonin: beyond circadian regulation - exploring its diverse physiological roles and therapeutic potential
- Review, Nor, NA
*CLOCK↝, In mammals, melatonin primarily serves to regulate the circadian rhythm system, which is essential for maintaining the sleep-wake cycle.
*BMD↑, Graphical Abstract
*cardioP↑,
*neuroP↑,
*Sleep↑,

1786- MEL,    What is known about melatonin, chemotherapy and altered gene expression in breast cancer (Review)
- Review, NA, NA
AntiTum↑, action of melatonin as an antitumor agen
Risk↓, well documented that melatonin diminishes the incidence of chemically induced cancers and is able to slow down the growth of certain hormone-responsive cancers
ChemoSen↑, numerous reports endorsing the beneficial use of melatonin during chemotherapy in clinical trials

1785- MEL,    Antitumoral melatonin-loaded nanostructured lipid carriers
- in-vitro, Var, NA
selectivity↑, MEL-NLC selectively induced cytotoxicity in several cancer cell lines while sparing healthy cells
TumCD↑,

1784- MEL,    Melatonin as adjuvant cancer care with and without chemotherapy: a systematic review and meta-analysis of randomized trials
- Review, NA, NA
Remission↑, Improved effect was found for complete response, partial response, and stable disease with RRs of 2.33 (95% CI = 1.29-4.20), 1.90 (1.43-2.51), and 1.51 (1.08-2.12), respectively

1783- MEL,    The efficacy and safety of melatonin in concurrent chemotherapy or radiotherapy for solid tumors: a meta-analysis of randomized controlled trials
- Review, Var, NA
Dose∅, dosage of melatonin used in the 8 included RCTs was 20 mg orally, once a day.
Remission↑, Melatonin significantly improved the complete and partial remission (16.5 vs. 32.6%; RR = 1.95, 95% CI, 1.49-2.54; P < 0.00001)
OS↑, as well as 1-year survival rate (28.4 vs. 52.2%; RR = 1.90; 95% CI, 1.28-2.83; P = 0.001)
radioP↑, dramatically decreased radiochemotherapy-related side effects

1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1↓,
CDK4↓,
CycB↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated

1781- MEL,    Melatonin in patients with cancer receiving chemotherapy: a randomized, double-blind, placebo-controlled trial
- Trial, Lung, NA
QoL↑, Patients in the melatonin-treated group had better adjusted HRQoL scores, with a slightly significantly better score (2.69 points, 95% confidence interval (CI)=0.01-5.38, p=0.049) being found in social well-being
OS∅, Median survival was 7.3 months (95% CI=3.42-11.14) without significant difference (lower survival in placebo group)
selectivity↑, A great amont of DNA damage marker was observed in the placebo-treated group, and this was associated with lower survival (r(2)=-0.656, p=0.02), implying the protective effect of melatonin in healthy cells.

1780- MEL,    Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing
- Review, Var, NA
*antiOx↑, Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy.
*toxicity↓,
ChemoSen↑,
*eff↑, melatonin was superior in preventing free radical destruction compared to other antioxidants, vitamin E, β-carotene, vitamin C, and garlic oil
*mitResp↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ATP↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ROS↓, most attractive property of melatonin is that its metabolites also regulate the mitochondrial redox status by scavenging ROS and RNS
*CardioT↓, melatonin has a protective effect on the heart without affecting DOX's antitumor activity,
*GSH↑, improving the de novo synthesis of glutathione (GSH) by promoting the activity of gamma-glutamylcysteine synthetase
*NOS2↓, melatonin inhibits the production of nitric oxide synthase (NOS)
*lipid-P↓, lipid peroxidation was reduced after melatonin treatment (role in induces organ failure)
eff↑, but it also enhances its antitumor activity more than vitamin E
*HO-1↑, melatonin upregulates heme oxygenase-1 (HO-1) (role in induces organ failure)
*NRF2↑, decreased bladder injury and apoptosis due to the upregulation of Nrf2 and nuclear transcription factor NF-κB expression
*NF-kB↑,
TumCP↓, significantly reduced cell proliferation
eff↑, Pretreatment with melatonin effectively preserved the ovaries from cisplatin-induced injury
neuroP↑, Melatonin has neuroprotective roles in oxaliplatin-induced peripheral neuropathy

1778- MEL,    Melatonin: a well-documented antioxidant with conditional pro-oxidant actions
- Review, Var, NA - Review, AD, NA
*ROS↓, melatonin and its metabolic derivatives possess strong free radical scavenging properties.
*antiOx↓, potent antioxidants against both ROS (reactive oxygen species) and RNS (reactive nitrogen species). reduce oxidative damage to lipids, proteins and DNA under a very wide set of conditions where toxic derivatives of oxygen are known to be produced.
ROS↑, a few studies using cultured cells found that melatonin promoted the generation of ROS at pharmacological concentrations (μm to mm range) in several tumor and nontumor cells; thus, melatonin functioned as a conditional pro-oxidant.
selectivity↑, melatonin functions as a prooxidant in cancer cells where it aids in the killing of tumor cells
Dose↑, Melatonin levels in the nucleus and mitochondria reached saturation with a lower dose of 40 mg/kg body weight, with no further accumulation under higher doses of injected melatonin
*mitResp↑, improves mitochondrial respiration and ATP production, thereby reducing electron leakage and ROS generation
*ATP↑,
*ROS↓,
eff↑, melatonin protects mitochondrial function in the brain of Alzheimer's patients through both MT1/MT2 dependent and independent mechanisms
ROS↑, Cytochrome P450 utilizes melatonin as a substrate to generate ROS in mitochondria (melatonin concentration ranges from 0.1 to 10 uM)
Dose↑, melatonin at high concentrations (10-1000uM ) was able to promote ROS generation and lead to Fas-induced apoptosis in human leukemic Jurkat cells. Concentrations of <10uM , melatonin did not induce significant ROS generation in these cancer cells
*toxicity∅, High levels of melatonin (uM to mM) did not cause cytotoxicity in several types of nontumor cells
ROS↑, lower concentrations of melatonin (0.1-10uM ), which exhibited antioxidant action in HepG2 cells within 24 hr, became pro-oxidant after 96 hr of treatment, as indicated by the increase of GSH with 24hr and depletion after 96 hr.
eff↓, Finally, a compound, chlorpromazine, which specifically interrupts the binding of melatonin to calmodulin [188], prevented melatonin-induced AA release and ROS generation;
ROS↝, 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
Dose↑, decline of melatonin production with age may render it more beneficial to supplement melatonin to the aging population to improve health by reducing free radical damage
other↑, melatonin intake has the potential to improve cardiac function, inhibit cataract formation, maintain brain health, alleviate metabolic syndrome, obesity and diabetes,reduce tumorigenesis, protect tissues against ischemia

1777- MEL,    Melatonin as an antioxidant: under promises but over delivers
- Review, NA, NA
*ROS↓, uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances
*Fenton↓, reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions
*antiOx↑, credible evidence to suggest that melatonin should be classified as a mitochondria-targeted antioxidant
*toxicity∅, uncommonly high-safety profile of melatonin also bolsters this conclusion.
*GPx↑, melatonin was found to stimulate antioxidative enzymes including glutathione peroxidase and glutathione reductase
*GSR↑,
*GSH↑, melatonin upregulates the synthesis of glutathione
*NO↓, neutralize nitrogen-based toxicants, i.e., nitric oxide
*Iron↓, Melatonin chelates both iron (III) and iron (II), which is the form that participates in the Fenton reaction to generate the hydroxyl radical
*Copper↓, copper-chelating ability of melaton
*IL1β↓, significant reductions in plasma cardiac troponin 1, interleukin 1 beta, inducible nitric oxide synthase (iNOS) and caspase 3 due to melatonin
*iNOS↓,
*Casp3↓,
*BBB↑, melatonin readily crosses the blood-brain barrier;
*RenoP↑, Published reports haveshown that the lung,231, 232 liver, 233- 235 kidney,236 pancreas,237 intestine,238 urinary bladder,239,240 corpus cavernosum,241 skeletal muscle242, 243 spinal cord244, 245 and stem cells246 are alsoprotected by melatonin.
chemoP↑, Melatonin has not been found to interfere with the efficacy of prescription drugs. Doxorubicin, if given it in combination with melatonin may allow the use of a larger dose with greater efficacy.
*Ca+2↝, Moreover, melatonin regulates free Ca2+ movement intracellularly
eff↑, elatonin was found to exaggerate the cancer inhibiting actions of pitavastatin270 and pravastatin271 against breast cancer in experimental studies
*PKCδ?, major targets by which melatonin reduces methamphetamine-related neuronal damage is due to the inhibition of the PKCδ gene
ChemoSen↑, at least some cases melatonin reduces the toxicity of these pharmacological agents in normal cells256, 289, 290 while enhancing the cancer-killing actions (also, see below) of conventional chemotherapeutic agents.256, 291-293
eff↑, TRAIL was combined with melatonin for the treatment of A172 and U87 human glioblastoma cells, however, apoptotic cell death was greatly exaggerated over that caused by TRAIL alone
Akt↓, in GBM: observed effect was related to a modulation of protein kinase c which reduced Akt activation resulting in a rise in death receptor 5 (DR5) levels;
DR5↑,
selectivity↑, The pro-oxidant action of melatonin is common in cancer cells while in normal cells the indoleamine is a powerful antioxidant.
ROS↑, cancer cells
eff↑, human lung adenocarcinoma cells (SK-LV-1) showed that melatonin also increased their sensitivity to the chemotherapy, cisplatin.

1776- MEL,    Therapeutic strategies of melatonin in cancer patients: a systematic review and meta-analysis
- Review, NA, NA
Remission↑, tumor remission rate in the MLT group was significantly higher than that in the control group
OS↑, MLT group had an overall survival rate of 28.24% (n=294/1,041), which was greatly increased compared with the control group (RR =2.07; 95% CI, 1.55–2.76; P<0.00001; I2=55%)
neuroP↑, MLT could effectively reduce the incidence of neurotoxicity
VEGF↓, by the downregulation of vascular endothelial growth factor (VEGF)
KISS1↑, MLT could suppress the metastasis of triple-negative breast cancer by inducing KISS1 expression
TumCP↓, MLT can significantly inhibit the proliferation of cancer cells
ChemoSideEff↓, while reducing the incidence of side effects in chemotherapy or radiotherapy
radioP↑, In the 20 randomized trials included, MLT was beneficial to reduce multiple side effects of radiotherapy and chemotherapy
Dose∅, mostly 20 mg/day and taken orally and taken at night, respectively
*ROS↓, Preclinical experimental research has confirmed that MLT was capable of scavenging ROS and repairing damaged DNA to exert antitumor effects
DNArepair↑,
ROS↑, The mechanisms of MLT exerting antitumor effect might involve with other pathways, such as antiangiogenesis and pro-oxidant

1775- MEL,  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↑, According to the findings, it was shown that melatonin co-treatment alleviates the ototoxic damage induced by chemotherapy and radiotherapy
radioP↑,
antiOx↑, melatonin may exert its otoprotective effects via its anti-oxidant, anti-apoptotic, and anti-inflammatory activities and other mechanisms.
Inflam↑,

1063- MEL,    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↓,

1042- MEL,    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↓, we found that lung cancer cells harboring the KRAS mutation exhibited a higher level of programmed death ligand 1 (PD-L1). However, treatment with melatonin substantially downregulated PD-L1
YAP/TEAD↓,
TAZ↓,
TumCG↓, mouse

995- MEL,    Melatonin Treatment Triggers Metabolic and Intracellular pH Imbalance in Glioblastoma
- vitro+vivo, GBM, NA
LDHA↓,
MCT4↓,
lactateProd↓,
i-pH↓, decrease in intracellular pH: melatonin treatment induced a pH reversal with intracellular acidosis parallel to a downregulation in glycolysis in GBM.
ROS↑,
ATP↓,
TumCD↑, cytotoxic effects on GBM were due, at least in part, to intracellular pH modulation
TumCCA↑, cell cycle arrest at G0/G1 in both GBM1A and QNS120 and G2/M in GBM1A
PDH↓, decrease in pyruvate dehydrogenase (PDH) expression for both cell lines at aMT 3.0 mM
Glycolysis↓,
GlucoseCon↓,
TumCG↓, in vivo

971- MEL,    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↓, inhibit expression of HIF-1 alpha protein under both normoxic and hypoxic conditions in DU145, PC-3, and LNCaP prostate cancer cells without affecting HIF-1 alpha mRNA levels
VEGF↓,
p‑p70S6↓,

3863- RES,  MEL,  VitA,RetA,    Target Enzymes Considered for the Treatment of Alzheimer's Disease and Parkinson's Disease
- Review, AD, NA - Review, Park, NA
*ADAM10↑, resveratrol, with a polyphenol framework found in grape skin, peanut, and pomegranates, has been reported to be applied for the treatment of ND to enhance ADAM10 expression indirectly.
*ADAM10↑, In short, ADAM10 activity could be elevated by biological molecules such as XBP-1, SOX-2, PAX2, and melatonin.
*ADAM10↑, Small molecules such as bryostatin-1, retinoic acid, acitretin, Am80, and phlogacantholide C and multiple natural products (i.e., resveratrol, gemfibrozil, and etazolate) have been reported as upregulators of ADAM10.

1313- VitD3,  MEL,    The effects of melatonin and vitamin D3 on the gene expression of BCl-2 and BAX in MCF-7 breast cancer cell line
- in-vitro, BC, MCF-7
BAX↑, upregulation of Bax gene
Bcl-2↓,
Bax:Bcl2↑, Bax/BCL-2 ratio was increased significantly
eff↑, treatment with melatonin and vitamin D3 inhibits the proliferation and induced apoptosis in breast cancer cells


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 22

Results for Effect on Cancer/Diseased Cells:
Ac-histone H3↑,1,   Akt↓,2,   angioG↓,1,   AntiCan↑,2,   antiOx↑,2,   AntiTum↑,1,   Apoptosis↓,1,   Apoptosis↑,3,   ATP↓,1,   BAX↑,4,   Bax:Bcl2↑,1,   Bcl-2↓,4,   BioAv↝,1,   CAIX↑,1,   Casp3↑,3,   Casp9↑,1,   Catalase↑,1,   CD4+↑,1,   CDK4↓,2,   chemoP↑,3,   ChemoSen↑,5,   ChemoSideEff↓,2,   CHOP↑,1,   COX2↓,1,   CycB↓,1,   cycD1↓,1,   DNAdam↑,1,   DNArepair↑,2,   Dose↓,1,   Dose↑,3,   Dose∅,4,   DR5↑,1,   E-cadherin↑,1,   eff↓,1,   eff↑,12,   ER Stress↑,1,   FOXP3↓,1,   GlucoseCon↓,1,   GLUT1↑,1,   GLUT3↑,1,   Glycolysis↓,1,   GPx↑,1,   GSH↓,1,   HDAC1↓,1,   Hif1a↓,2,   IGF-1R↓,1,   IL1β↓,1,   IL6↓,2,   IL8↓,1,   Inflam↓,1,   Inflam↑,1,   JNK↑,1,   Ki-67↓,1,   KISS1↑,1,   lactateProd↓,1,   LDHA↓,1,   MAPK↑,1,   MCT4↓,1,   MMP13↓,1,   MMP2↓,1,   MMP9↓,1,   neuroP↑,2,   NF-kB↓,1,   NK cell↑,2,   NO↓,1,   OS↑,4,   OS∅,1,   other↑,1,   P21↑,1,   p27↑,1,   P53↑,1,   p‑p70S6↓,1,   PCNA↓,1,   PD-L1↓,1,   PDH↓,1,   i-pH↓,1,   PI3K↓,1,   PTEN↑,1,   PUMA↑,1,   QoL↑,2,   radioP↑,5,   RadioS↑,1,   RANKL↓,1,   Remission↑,3,   Risk↓,2,   ROS↑,10,   ROS↝,1,   selectivity↑,5,   SOD↑,1,   STAT3↓,1,   T-Cell↑,1,   TAZ↓,1,   Th1 response↑,1,   TNF-α↓,1,   TNF-α↑,1,   Treg lymp↓,1,   Trx1↓,1,   TumCCA↑,1,   TumCD↑,3,   TumCG↓,2,   TumCG↑,1,   TumCMig↓,1,   TumCP↓,3,   tumCV↓,1,   TumMeta↓,1,   TumMeta↑,1,   TumVol↓,1,   VEGF↓,3,   Vim↓,1,   Warburg↓,1,   XBP-1↑,1,   YAP/TEAD↓,1,  
Total Targets: 112

Results for Effect on Normal Cells:
ADAM10↑,3,   antiOx↓,1,   antiOx↑,3,   AntiTum↑,1,   ATP↑,2,   BBB↑,1,   BMD↑,1,   Ca+2↝,1,   cardioP↑,1,   CardioT↓,1,   Casp3↓,1,   Catalase↑,1,   CLOCK↝,1,   Copper↓,1,   eff↑,1,   Fenton↓,1,   GPx↑,2,   GSH↑,3,   GSR↑,1,   HO-1↑,1,   IL1β↓,1,   iNOS↓,1,   Iron↓,1,   lipid-P↓,1,   mitResp↑,2,   neuroP↑,1,   NF-kB↑,1,   NO↓,1,   NOS2↓,1,   NRF2↑,1,   PKCδ?,1,   RenoP↑,1,   ROS↓,6,   Sleep↑,1,   SOD↑,1,   toxicity↓,1,   toxicity∅,2,  
Total Targets: 37

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:122  Target#:%  State#:%  Dir#:%
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