glucose Cancer Research Results
glucose, glucose: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*antiOx↑, LA has long been touted as an antioxidant,
*glucose↑, improve glucose and ascorbate handling,
*eNOS↑, increase eNOS activity, activate Phase II detoxification via the transcription factor Nrf2, and lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*NRF2↑,
*MMP9↓,
*VCAM-1↓,
*NF-kB↓,
*cardioP↑, used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits,
*cognitive↑,
*eff↓, The efficiency of LA uptake was also lowered by its administration in food,
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies;
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑, LA markedly increases intracellular glutathione
(GSH),
*PKCδ↑, PKCδ, LA activates Erk1/2 [92,93], p38 MAPK [94], PI3 kinase [94], and Akt
*ERK↑,
*p38↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN [95],
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, stimulate GLUT4 translocation
*GLUT1↑, LA-stimulated translocation of GLUT1 and GLUT4.
*Inflam↓, LA as an anti-inflammatory agent
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*glucose↑, The compound enhances metabolic health by improving glucose uptake and insulin sensitivity and offers cardiovascular protection through its anti-inflammatory and lipid-lowering effects.
*cardioP↑,
*Inflam↓,
*lipid-P↓,
GutMicro↑, Suppression of gastritis caused by Helicobacter pylori (H. pylori)
TumCP↓, cinnamaldehyde could inhibit the proliferation, change the morphology, promote apoptosis, and reduce the invasiveness and migratory ability of MDA-MB-231 cells.
Apoptosis↑,
TumCI↓,
TumCMig↓,
BAX↑, cinnamaldehyde upregulated BAX and p53 expression, whereas it downregulated BCL2 and cellular inhibitor of apoptosis 2 (CIAP2) expression.
P53↑,
Bcl-2↓,
IAP1↓,
PI3K↓, cinnamaldehyde significantly suppressed the transcriptional activity of PI3K/AKT
Akt↓,
*ROS↓, Other studies have shown that cinnamaldehyde can also enhance the anti-oxidant defense against ROS generated under hyperglycemic conditions, thereby preventing the loss of islet β cells and exerting a hypoglycemic effect
*NRF2↑, Studies have found that cinnamaldehyde can decrease the levels of nicotinamide adenine dinucleotide phosphate (NADPH) enzyme, reduce ROS, change the mitochondrial membrane potential, reduce caspase pathway conduction, and promote the reduction of apo
*NF-kB↓, It has been found that cinnamaldehyde exerts a therapeutic effect on psoriasis-like inflammation by inhibiting the NF-κB pathway
NF-kB↑, Analysis of the inhibitory effect of cinnamaldehyde on tumor growth demonstrated that blockage of the NF-κB pathway led to inhibition of the growth and spread of breast cancer cells, resulting in an anti-cancer effect.
eff↑, kaempferol could reverse the drug resistance of HCT8-R cells to 5-Fu, suggesting that kaempferol alone or in combination with 5-Fu has the potential to treat colorectal cancer
GlucoseCon↓, kaempferol treatment significantly reduced glucose uptake and lactic acid production in drug-resistant colorectal cancer cells.
lactateProd↓,
PKM2↓, kaempferol promotes the expression of microRNA-326 (miR-326) in colon cancer cells, and miR-326 could inhibit the process of glycolysis by directly targeting pyruvate kinase M2 isoform (PKM2) 3′-UTR (untranslated region) to inhibit PKM2
Glycolysis↓, Kaempferol Promotes 5-Fu Sensitivity by Inhibiting Glycolysis
glucose↑, kaempferol treatment dramatically increased the content of glucose in HCT8-R cell culture medium (Figure 3E) and decreased the content of lactate (Figure 3F), suggesting that kaempferol might promote the 5-Fu sensitivity by inhibiting glycolysis.
Showing Research Papers: 1 to 3 of 3
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3
Pathway results for Effect on Cancer / Diseased Cells:
Core Metabolism/Glycolysis ⓘ
glucose↑, 1, GlucoseCon↓, 1, Glycolysis↓, 1, lactateProd↓, 1, PKM2↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 1, BAX↑, 1, Bcl-2↓, 1, IAP1↓, 1,
DNA Damage & Repair ⓘ
P53↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Migration ⓘ
TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Immune & Inflammatory Signaling ⓘ
NF-kB↑, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1,
Total Targets: 18
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 1, lipid-P↓, 1, NRF2↑, 2, ROS↓, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, glucose↑, 2,
Cell Death ⓘ
Akt↑, 1, MAPK↑, 1, p38↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, PI3K↑, 1, PTEN↓, 1,
Migration ⓘ
MMP9↓, 1, PKCδ↑, 1, VCAM-1↓, 1,
Angiogenesis & Vasculature ⓘ
eNOS↑, 1,
Barriers & Transport ⓘ
BBB↑, 1, GLUT1↑, 1, GLUT4↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 2, NF-kB↓, 2,
Drug Metabolism & Resistance ⓘ
eff↓, 1,
Functional Outcomes ⓘ
cardioP↑, 2, cognitive↑, 1,
Total Targets: 26
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#:2
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