glucose Cancer Research Results
glucose, glucose: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*antiOx↑, mainly shown as anti-oxidant, liver and kidney protection, anti-bacterial, anti-tumor, regulation of glucose metabolism and lipid metabolism, anti-inflammatory, protection of the nervous system,
*hepatoP↑,
*RenoP↑,
AntiTum↑,
*glucose↝,
*Inflam↓,
*neuroP↑,
*ROS↓, ↓Active oxygen (ROS) , ↓Keap1,↑Nrf2, ↑SOD, ↑CAT, ↑Glutathione Peroxidase (GSH-Px), ↑Glutathione (GSH), ↓MDA
*Keap1↓,
*NRF2↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*MDA↓,
*p‑ERK↑, ↑ERK1/2 phosphorylation
*GRP78/BiP↑, ↑Glucose regulatory protein 78 (GRP78)
*CHOP/DDIT3↑, ↑C/EBP homologous protein (CHOP)
*GRP94↑, ↑Glucose Regulatory Protein 94 (GRP94)
*Casp3↓, ↓Caspase-9/Caspase-3
*Casp9↓,
*HGF/c-Met↑, ↑Hepatocyte Growth Factor (HGF)
*TNF-α↓, ↓Tumor Necrosis Factor-α (TNF-α)/Interferonγ (IFN-γ)
*TLR4↓, ↓TLR4
*MAPK↓, ↓MAPK signal pathway
*IL1β↓, ↓Interleukin 1β (IL-1β)/Interleukin 6 (IL-6)
*iNOS↓, ↓Inducible Nitric Oxide Synthase (iNOS)
TCA↓, ↓Tricarboxylic acid cycle (TCA) ↓Glycolysis
Glycolysis↓,
Bcl-2↓, ↓Anti-apoptotic gene Bcl-2/Bcl-XL
BAX↑, ↑Pro-apoptotic gene Bax/Bcl-XS/Bad
MAPK↑, ↑p38 mitogen-activated protein kinase (p38 MAPK)
JNK↑, ↑c-Jun N-terminal Kinase (JNK)
CSCs↓, ↓Stem cell marker genes Nanog, POU5F1, Sox2, CD44, Oct4
Nanog↓,
SOX2↓,
CD44↓,
OCT4↓,
P53↑, ↑P53
P21↑, ↑p21
*SOD1↑, ↑CuZnSOD (SOD1)/MnSOD (SOD2)
*AGEs↓, ↓Glycosylation end products (AGEs)
*GLUT2↑, ↑Glucose Transporter 2 (GLUT2)
*HDL↑, ↑High-density lipoprotein (HDL)
*Fas↓, ↓Fatty acid synthase (FAS)
*HMG-CoA↓, ↓β-hydroxy-β-methylglutamyl-CoA (HMG-CoA) reductase
*NF-kB↓, ↑NF-κB signaling pathway
*HO-1↓, ↑Nrf2/HO-1 signaling pathway
*COX2/PTGS2↓, ↓Cyclooxygenase-2 (COX-2)
*TLR4↓, ↓Toll-like receptor 4 (TLR4)
*BioAv↑, One route may be immediate absorption in the stomach or upper gastrointestinal tract, and the other route may be slowly absorbed throughout the small intestine.
*BioAv↝, It indicates that the bioavailability of CGA is closely related to the metabolic capacity of the organism's gut flora
TumCP↓, CGA also inhibits the proliferation, migration, and invasion of cancer cells.
TumCMig↓,
TumCI↓,
*neuroP↑, Chlorogenic acid (CGA) is one of the most common dietary polyphenols with neuroprotective effects.
*BioAv↑, CGA were used to prepare a new flowerlike selenium nanocluster (TGN-CGA@SeNCs) for enhancing the bioavailability of CGA.
*GutMicro↑, At the same concentration, the CGA-modified selenium nanocluster (CGA@SeNCs) and TGN-CGA@SeNCs showed better function in ameliorating the gut microbiota disorder.
*BBB↑, Notably, only TGN-CGA@SeNCs can transport through the blood-brain barrier (BBB)
*Aβ↓, and TGN-CGA@SeNCs showed better effects than CGA@SeNCs in regulating Aβ aggregation and improving brain glucose homeostasis.
*glucose↝,
*Inflam↓, May reduce immune cell mediated inflammation and oxidative stress, but has very low oral
bioavailability.
*ROS↓,
*BioAv↓,
*GutMicro↑, May exert beneficial effects through modulation of the intestine/microbiome
*neuroP↑, Neuroprotective Benefit: Can protect against onset of inflammatory and oxidative damage by
mitigating immune cell activation in animal models.
*glucose↝, May help regulate glucose homeostasis, have anti-thrombotic effects, and improve tolerability of chemotherapy, but benefits are limited by poor oral bioavailability.
*AntiThr↑,
*chemoP↑,
*Half-Life↝, Half-life: Varies with preparation (~1-3 hours in rats)
*BBB∅, BBB: Not penetrant
*AntiAge↑, Diets rich in fucoidan associated with increased lifespan and lower cancer incidence.
Risk↑,
| - |
Review, |
Var, |
NA |
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|
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- |
Review, |
Diabetic, |
NA |
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*IRes↓, number of synthetic and natural insulin sensitizers, including inositol, have been recognized to exert both anti-diabetic as well as anti-cancer properties.
*AntiDiabetic↑,
*glucose↝, beneficial effect of inositol in fostering glucose homeostasis as well as in antagonizing cancer growth.
AntiCan↑,
PI3K↓, NOSITOL INHIBITS THE PI3K/AKT PATHWAY IN CANCER CELLS
Akt↓,
Glycolysis↓, On the contrary, in cancer cells, IPGs and myo-Ins inhibits Akt reducing both glycolysis and glucose entry in the cell, while re-establishing the oxidative degradation of carbohydrates along the TCA.
STK11/LKB1↑, As inositol enhances specifically the LKB1 activity, it is worth noting that the AMPK-related anticancer activities are tightly dependent of that pathway
*FASN↓, Inositol inhibits fatty acids biosynthesis and reduces plasma LDL-cholesterol and non-esterified fatty acids (NEFA) levels [74-76].
*LDL↓,
*FFA/NEFA↓,
*ROS↓, Myo-Ins counteracts oxidative damage in fish exposed to environmental oxidative stress
ROS↑, anti-oxidant effects seem to be contextdependent, given that in cancer cells inositol actually increases free radical production
IGF-1↓, Furthermore, myoIns may likely inhibit IGF-1 release downstream of the induced inhibition
*glucose↝, Myo-inositol, the most common stereoisomer of inositol, plays an important role in many physiological processes, such as cell signaling, regulation of glucose and lipid metabolism, and protection of cells against oxidative stress.
*lipid-P↓,
*ROS↓,
*BioAv↑, characterized by high oral bioavailability and is primarily eliminated via the kidneys.
*hepatoP↑, Preclinical studies have shown that myo-inositol has hepatoprotective potential, reducing oxidative stress, inflammation, and lipid accumulation in hepatocytes,
*Inflam↓,
*MMP↑, Recent findings suggest that it contributes to the stabilization of mitochondrial membranes and enhances ATP production efficiency,
*ATP↑,
*GutMicro↑, Evidence indicates that myo-inositol may influence intestinal microbiota composition, enhancing populations of beneficial bacterial strains while reducing endotoxemia linked to non-alcoholic fatty liver disease
*Dose↝, a significant portion of the body’s requirement is also supplied by the diet-rich sources, including fruits, whole grains, legumes, and nuts.
*Half-Life↝, Studies on rats has revealed that the highest plasma concentrations were observed within 1–2 h after oral intake, while the half-life ranged from 4 to 8 h.
*BioAv↑, In the case of intravenous administration, higher bioavailability and faster tissue distribution were achieved. intravenous administration of myo-inositol is rare
*eff↑, myo-inositol supplementation may potentially synergize with antioxidants (e.g., vitamin E, curcumin), enhancing their protective effects on the liver and other organs exposed to oxidative stress
*hepatoP↑, Myo-inositol may exert hepatoprotective effects through several biological mechanisms. A key role is played by its involvement in lipid metabolism regulation, modulation of oxidative stress, and influence on insulin signaling.
*SOD↑, Moreover, myo-inositol and its derivatives (including D-chiro-inositol) affect the activation of antioxidant enzymes such as superoxide dismutase (SOD) and catalase, thereby limiting oxidative damage to hepatocytes
*Catalase↑,
*Casp3↓, inhibit the expression of apoptosis markers such as caspase-3,
*ALAT↓, decreased activity of transaminases (ALT, AST).
*AST↓,
*AMPK↑, regulation of lipid metabolism through the activation of AMP-activated protein kinase (AMPK) and downregulation of sterol regulatory element-binding proteins (SREBPs).
*SREBP1/SREBF1↑,
*NA↑,
other↑, Deregulated inositol metabolism has been recorded in a number of diseases, including cancer, where inositol modulates different critical pathways.
p‑pRB↓, Inositols inhibit pRB phosphorylation, fostering the pRB/E2F complexes formation and blocking progression along the cell cycle.
TumCCA↑,
PI3K↓, Inositols reduce PI3K levels, thus counteracting the activation of the PKC/RAS/ERK pathway downstream of PI3K activation.
Akt↓, Akt activation is severely impaired upon inositol addition
ERK↓, Downregulation of both Akt and ERK leads consequently to NF-kB inhibition and reduced expression of inflammatory markers (COX-2 and PGE2).
NF-kB↓,
COX2/PTGS2↓,
PGE2↓,
PSEN1/PS1↓, Remarkably, inositol-induced downregulation of presenilin-1 interferes with the epithelial-mesenchymal transition and reduces Wnt-activation, β-catenin translocation, Notch-1, N-cadherin, and SNAI1 release.
EMT↓,
Wnt↓,
β-catenin/ZEB1↓,
NOTCH1↓,
N-cadherin↓,
Snail↓,
E-cadherin↑, upregulating Focal Adhesion Kinase and E-cadherin and decreasing Fascin and Cofilin, two main components of pseudopodia, leading hence to invasiveness impairment.
fascin↓,
Cofilin↓,
MMPs↓, inositol-induced inhibition on metalloproteinases and ROCK1/2 release
ROCK1↓,
Dose↝, A mixed western diet provides the human adult with approximately 1 g of total inositol per day. it may be surmised that in western countries low-vegetable consumers may suffer from a relative deficiency of myo-Ins
other↝, InsP6 is often referred to as an antinutrient [20] responsible for iron deficiencies mostly in underdeveloped countries, it should be emphasized that InsP6 displays its antinutritional effects only when the diet is already deprived of trace elements
selectivity↑, specific for cancer cells, given that both InsP6 and myo-Ins did not promote apoptosis in normal cells.
*ROS↓, Myo-Ins counteracts oxidative damage in fish exposed to environmental stresses [114] and significantly inhibits systemic markers of oxidative stress in gynecological patients
*lipid-P↓, thus preventing formation of ADP-iron-oxygen complexes that trigger lipid peroxidation
ROS↑, antioxidant property of inositol is strictly context-dependent as, under specific conditions, both myo-Ins and InsP6 may increase free radical production
NK cell↑, inositol hexakisphosphate and myo-Ins enhance NK activity in mice treated with 1,2-dimethylhydrazine (DMH),
Imm↑, enhancement of immune function
TNF-α↓, InsP6 also modulates the transcription genes for TNF by decreasing it and its receptors in colon cancer cells
ChemoSen↑, inositol hexakisphosphate may potentiate the anticancer effects of conventional chemotherapy in preventing the successful development of cancer implants
Dose↑, Mild side effects (mostly represented by nausea or diarrhea) are reported in a small fraction of subjects, only for doses up to 12 g/day
toxicity↓,
QoL↑, where InsP6 plus myo-Ins treatment is associated with appreciable reduction in tumor burden and improved quality of life
chemoP↑, , if inositols were added along with conventional chemotherapy, colon cancer patients experienced significantly less side effects than controls, as reported in a pilot study
OS↑, Furthermore, prolonged survival and better quality of life have been obtained in some anecdotal cases of breast and lung cancer patients treated with InsP6 and myo-Ins
Dose↝, A study enrolling 26 smokers showed that myo-Ins in a daily dose up to 18 g/p.o. is safe and well tolerated, while inducing a significant regression of individual pulmonary dysplastic lesions
Insulin↓, downregulation of insulin levels, improved glucose utilization through the oxidative cycle, and inhibition of lipogenesis).
glucose↝,
lipoGen↓,
eff↑, There is a widespread consensus suggesting that InsP6 and myo-Ins act synergistically when added in association.
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
PSEN1/PS1↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
ROS↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
Insulin↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↝, 1, Glycolysis↓, 2, lipoGen↓, 1, STK11/LKB1↑, 1, TCA↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, BAX↑, 1, Bcl-2↓, 1, JNK↑, 1, MAPK↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1, other↝, 1, p‑pRB↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD44↓, 1, CSCs↓, 1, EMT↓, 1, ERK↓, 1, IGF-1↓, 1, Nanog↓, 1, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 2, SOX2↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
Cofilin↓, 1, E-cadherin↑, 1, fascin↓, 1, MMPs↓, 1, N-cadherin↓, 1, ROCK1↓, 1, Snail↓, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1, β-catenin/ZEB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, Imm↑, 1, NF-kB↓, 1, NK cell↑, 1, PGE2↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↑, 1, Dose↝, 2, eff↑, 1, selectivity↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 1, chemoP↑, 1, OS↑, 1, QoL↑, 1, Risk↑, 1, toxicity↓, 1,
Total Targets: 59
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
FFA/NEFA↓, 1, IRes↓, 1, NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 2, GPx↑, 1, GSH↑, 1, HDL↑, 1, HO-1↓, 1, Keap1↓, 1, lipid-P↓, 2, MDA↓, 1, NRF2↑, 1, ROS↓, 5, SOD↑, 2, SOD1↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, AMPK↑, 1, FASN↓, 1, glucose↝, 5, GLUT2↑, 1, HMG-CoA↓, 1, LDL↓, 1, SREBP1/SREBF1↑, 1,
Cell Death(tgid=5) ⓘ
Casp3↓, 2, Casp9↓, 1, Fas↓, 1, HGF/c-Met↑, 1, iNOS↓, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, GRP78/BiP↑, 1, GRP94↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
p‑ERK↑, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, BBB∅, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, IL1β↓, 1, Inflam↓, 3, NF-kB↓, 1, TLR4↓, 2, TNF-α↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv↝, 1, Dose↝, 1, eff↑, 1, Half-Life↝, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, GutMicro↑, 3,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, chemoP↑, 1, hepatoP↑, 3, neuroP↑, 3, RenoP↑, 1,
Total Targets: 62
Scientific Paper Hit Count for: glucose, glucose
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#:1278 State#:% Dir#:4
wNotes=on sortOrder:rid,rpid
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