VitE Cancer Research Results
VitE, Vitamin E (trolox): Click to Expand ⟱
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Vitamin E is best known for its ability to neutralize free radicals and reduce oxidative damage to lipids, proteins, and DNA.
• α‐Tocopherol Transfer Protein (TTPA)
– Role: Transfers vitamin E (α‐tocopherol) between membranes.
Trolox is a water-soluble analog of vitamin E
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Scientific Papers found: Click to Expand⟱
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,
RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP/DDIT3↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration
Showing Research Papers: 1 to 2 of 2
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↓, 1, CYP1A1↓, 1, GPx↓, 1, GSH↓, 2, GSR↓, 1, GSTs↓, 1, HO-1↓, 1, NQO1↓, 1, NRF2↓, 1, ROS↑, 2, SOD↓, 1, SOD2↓, 1, VitC↓, 1, VitE↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
SIRT1↓, 1,
Cell Death(tgid=5) ⓘ
p‑Akt↓, 1, Bcl-2↓, 1, Casp1↓, 1, Casp3↑, 2, Casp8↑, 1, Cyt‑c↑, 1, DR5↑, 1, Fas↑, 1, FasL↑, 1, HGF/c-Met↓, 1, p‑JNK↑, 1, MAPK↓, 1, p‑MDM2↓, 1, p‑p38↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
H3↓, 1, H4↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, p‑eIF2α↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3II↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
PARP↑, 1, PCNA↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD34↓, 1, cFos↑, 1, EMT↓, 1, HDAC↓, 1, mTOR↓, 1, NOTCH1↓, 1, p‑PI3K↓, 1, PTEN↓, 1, p‑Src↓, 1, STAT3↓, 1, p‑STAT6↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
AXL↓, 1, Cdc42↓, 1, CEA↓, 1, CLDN1↓, 1, E-cadherin↓, 1, FAK↓, 1, ITGB1↓, 1, MET↓, 1, p‑MET↓, 1, MMP2↓, 1, N-cadherin↓, 1, Rac1↓, 1, Rho↓, 1, Snail↓, 1, Tyro3↓, 1, Vim↑, 1, ZO-1↑, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
EGFR↑, 1, VEGF↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
ASC↓, 1, ICAM-1↓, 1, IKKα↓, 1, IL2↑, 1, IL6↓, 1, NF-kB↓, 1, p‑p65↓, 1, PD-1↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1, NLRP3↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, ChemoSen↑, 2, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, CEA↓, 1, EGFR↑, 1, IL6↓, 1, NSE↓, 1,
Functional Outcomes(tgid=23) ⓘ
cachexia↓, 1, chemoP↑, 2, QoL↑, 1, radioP↑, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 96
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
SpO2↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 2, Fenton↓, 1, GPx↑, 1, GSH↑, 1, GSTs↑, 1, HO-1↑, 1, lipid-P↓, 2, MDA↓, 1, MPO↓, 1, NOX4↓, 1, NRF2↑, 1, RNS↓, 1, ROS↓, 1, SOD↑, 2, TBARS↓, 1, VitE↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
NADPH↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Apoptosis↓, 1, Bcl-2↑, 1, Bcl-xL↑, 1, Casp3↓, 2, Casp9↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
PI3K↑, 1, STAT3↑, 1,
Migration(tgid=13) ⓘ
Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↑, 1, FOXP3↑, 1, HMGB1↓, 1, IL10↑, 2, IL1β↓, 2, IL4↑, 1, IL6↓, 1, Inflam↓, 1, JAK2↑, 1, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 2,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 2, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
OS↑, 1, Weight↑, 1,
Total Targets: 58
Scientific Paper Hit Count for: VitE, Vitamin E (trolox)
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#:% Target#:1252 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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