GLUT3 Cancer Research Results

GLUT3, GLUT3: Click to Expand ⟱

Source:

Type:

GLUT3 is a member of the glucose transporter family, which plays a crucial role in glucose uptake and metabolism in cells. In the context of cancer, GLUT3 has been found to be overexpressed in various types of tumors, including brain, breast, colon, and lung cancers.
GLUT3 is overexpressed in cancer cells compared to normal cells. This overexpression is thought to contribute to the increased glucose uptake and metabolism observed in cancer cells.

Scientific Papers found: Click to Expand⟱

3271-

ALA,

Decrypting the potential role of α-lipoic acid in Alzheimer's disease

Review,

AD,

*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models

3441-

ALA,

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

in-vivo,

AD,

mice

*tau↓, α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research
*GlucoseCon↑, chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brain
*GLUT3↑,
*GLUT4↑,
*VEGF↑,
*HO-1↑,
*Glycolysis↑, LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1).
*HK1↑, Our results indicated that the activity of HK was significantly increased after 10 mg/kg LA treatment.
*PGC-1α↑,
*Hif1a↑, found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.
*neuroP↑,

3547-

ALA,

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Review,

AD,

Review,

Park,

*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,

6216-

CUR,

Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials

Review,

Var,

TumCG↓, Curcumin can prevent tumor growth, angiogenesis, epithelial–mesenchymal transition, invasion, and metastasis by modulating the expression of tumor-related non-coding RNA (ncRNA)
angioG↓,
EMT↓,
TumCI↓,
TumMeta↓,
*GutMicro↑, curcumin plays a crucial role in regulating the gut microbiota via biotransformation of curcumin and its metabolites.
*BioAv↓, one of the primary drawbacks of taking curcumin alone is its low bioavailability, which appears to be caused by poor absorption, fast metabolism, and excretion
*HO-1↑, Curcumin is an efficient inducer of hemoxygenase-1 and a powerful inhibitor of reactive oxygen-generating enzymes, such as cyclooxygenase (COX), inducible nitric oxygen synthase (iNOS), lipoxygenase, and xanthine dehydrogenase/oxidase
*ROS↓,
*COX2↓,
*iNOS↓,
PKCδ↓, Curcumin is also a powerful inhibitor of protein kinase C (PKC), tyrosine kinase, epidermal growth factor receptor (EGFR), and IB kinase.
EGFR↓,
NF-kB↓, It suppresses NF-κB activation and the expression of oncogenes, such as c-jun, c-fos, c-myc, Akt, PI3K, cyclin-dependent kinase (CDK)
cJun↓,
cFos↓,
cMyc↓,
Akt↓,
PI3K↓,
CDK4↓,
*TNF-α↓, Continuous supplementation with nanocurcumin (two 40 mg capsules/day after a meal) for 3 months suppressed expression of inflammatory tumor necrosis factor-alpha (TNF-α), high sensitive protein with C-reactive protein (CRP), and interleukin-6 (IL-6)
*CRP↓,
*IL6↓,
MMP9↓, curcumin suppressed metastasis to the lung by suppressing NF-κB, MMP-9, COX-2, and vascular endothelial growth factor (VEGF) expression.
VEGF↓,
JAK↓, Curcumin remarkably inhibits JAK/STAT signaling by downregulating pro-inflammatory interleukins, such as IL-1, IL-2, IL-6, IL-8, IL-12, and MCP-1.
STAT↓,
IL1↓,
IL2↓,
IL6↓,
IL8↓,
IL12↓,
MCP1↓,
Apoptosis↑, It promotes apoptosis and ER stress by targeting phosphorylated protein kinase-like ER-resident kinase,
ER Stress↑,
5LO↓, inhibiting lipoxygenase and xanthine oxidase activity
XO↓,
*NRF2↑, The expression of nuclear factors erythroid 2-related factor (Nrf2) and heme oxygenase 1 (HO-1) is boosted by curcumin
*HO-1↑,
*AChE↓, Curcumin also inhibits the key enzyme acetylcholinesterase (AChE) and p300, a positive regulator of the Wnt/β-catenin pathway
*neuroP↑, Curcumin has also been suggested to prevent and cure neurotoxicity by replenishing dopamine and 3,4-dihydroxyphenylacetic acid levels.
*glucose↓, remarkably lowers blood glucose levels and improves insulin resistance by reducing hepatic glucose synthesis, inhibiting inflammatory reactions produced by hyperglycemia,
*GLUT2↑, boosting glucose transporters 2 (GLUT2), 3 (GLUT3), and 4 (GLUT4) gene expression, enhancing glucose uptake, and activating the AMPK signaling pathway.
*GLUT3↑,
*GLUT4↑,
*GlucoseCon↑,
*AMPK↑,
*BMD↑, Supplementation with nanomicelle curcumin (80 mg) alone or in combination with Nigella sativa oil (1000 mg) for 2–6 months increased plasma levels of miRNA-21 in postmenopausal women with low bone mass density.
*MDA↓, (1000 mg/day) for 8 weeks reduced serum levels of malondialdehyde (MDA) and high-sensitivity CRP (hs-CRP) and increased the total antioxidant capacity in 81 healthy postmenopausal women
*eff↑, Loriczova et al. demonstrated that iron (18 mg and 65 mg) supplementation along with curcumin (500 mg) reduces iron-induced systemic inflammation by reducing plasma levels of TNF-α
eff↑, high-dose vitamin C (25–100 g/day) along with oral nutrient supplementation including curcumin (1–3 g/day) had improved QoL and survival
P53↑, Curcumin was also reported to induce p53 and Bax expression in patients with colorectal cancer, causing apoptosis and DNA fragmentation and suppressing TNF-α and Bcl-2.
BAX↑,
DNAdam↑,
Bcl-2↓,
CSCs↓, The combination of curcumin, 5-fluorouracil (5-FU) and oxaliplatin (FOLFOX) in colorectal liver metastases reduced stem cell markers, such as aldehyde dehydrogenase and CD133.
ALDH↓,
CD133↑,

2310-

EGCG,

Epigallocatechin-3-gallate downregulates PDHA1 interfering the metabolic pathways in human herpesvirus 8 harboring primary effusion lymphoma cells

in-vitro,

lymphoma,

PEL

GLUT3↑, EGCG increased GLUT3 and decreased PDHA1 and GDH1 expression to disrupt glycolysis and glutaminolysis in PEL cells
PDHA1↓,
GDH↓,
ROS↑, Previously we have demonstrated that EGCG induces ROS generation and cell death in HHV8 harboring PEL cells
Glycolysis↓, EGCG induced PEL cell death may due to suppresses both the aerobic glycolysis and oxidative phosphorylation
OXPHOS↓,

1782-

MEL,

Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities

Review,

Var,

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/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↓,
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

3950-

Taur,

Taurine Supplementation as a Neuroprotective Strategy upon Brain Dysfunction in Metabolic Syndrome and Diabetes

Review,

Diabetic,

Review,

Stroke,

Review,

AD,

*Ca+2↝, taurine homeostasis can impact a number of biological processes, such as osmolarity control, calcium homeostasis, and inhibitory neurotransmission, and have been reported in both metabolic and neurodegenerative disorders.
*neuroP↑, taurine can afford neuroprotection in individuals with obesity and diabetes.
*other↝, Notably, both methionine and cysteine produced from protein degradation can generate taurine as an end-product
*pH↝, Taurine might counteract extreme mitochondrial pH fluctuations and help preserve mitochondrial physiology.
*ROS∅, Taurine is not able to act as a radical scavenger
eff↑, Taurine also decreased the activity of glutathione peroxidase and manganese-superoxide dismutase upon tamoxifen toxicity, which contributed to decreasing mitochondrial oxidative stress, measured through lipid peroxidation, protein carbonyl content, a
*MMP↑, In sum, taurine supplementation is proposed to improve the function of the mitochondria, contributing to the preservation of mitochondrial membrane potential, proton gradient, and matrix pH that are critical for energy metabolism and efficient oxidat
*Apoptosis↓, Taurine was found to prevent apoptosis upon many noxious challenges
*other↝, The most striking neuroprotective effects of taurine were observed on the reduction of apoptotic rates and the improvement of neurological outcomes upon brain ischemia.
*ER Stress↓, prevention of mitochondrial and endoplasmic reticulum (ER) stress.
*Bcl-xL↓, reduction of anti-apoptotic Bcl-xL and the increase of the pro-apoptotic Bax, preventing cytochrome C release from the mitochondria, and inhibiting the activation of calpain and caspase-3
*BAX↑,
*Cyt‑c↑,
*cal2↓,
*Casp3↓,
*UPR↓, prevent ischemia/hypoxia-induced endoplasmic reticulum (ER) stress by inhibiting the unfolded protein response via transcription factor 6 (ATF6), protein kinase R-like ER kinase (PERK), and inositol-requiring enzyme 1 (IRE1) pathways
*other↝, Altogether, one might speculate that taurine loss in patients with AD is linked to worsened cognitive deterioration.
*NF-kB↓, ameliorated the diabetes-induced increase of the transcription factor NF-κβ, involved in inflammatory processes, and the diabetes-induced reduction of Nrf2 and glucose transporters Glut1 and Glut3 in the brain.
*NRF2↑,
*GLUT1↑,
*GLUT3↑,
*memory↑, In mice fed a fat-rich diet, which develop metabolic syndrome, we recently demonstrated that 3% (w/v) taurine supplemented in the drinking water for 2 months prevented memory impairment

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 2, GPx↑, 2, GSH↑, 3, HK1↑, 1, HO-1↑, 5, lipid-P↓, 1, MDA↓, 1, NQO1↑, 1, NRF2↑, 4, ROS↓, 3, ROS∅, 1, SOD↑, 2, VitC↑, 1, VitE↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 2,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, glucose↓, 1, GlucoseCon↑, 4, GLUT2↑, 1, Glycolysis↑, 1, PDH↑, 1, PDKs↓, 1,

Cell Death ⓘ

Apoptosis↓, 1, BAX↑, 1, Bcl-xL↓, 1, Casp3↓, 1, Cyt‑c↑, 1, iNOS↓, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1, other↝, 3,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1, UPR↓, 1,

Proliferation, Differentiation & Cell State ⓘ

IGF-1↑, 1,

Migration ⓘ

Ca+2↓, 1, Ca+2↝, 1, cal2↓, 1, VCAM-1↓, 1,

Angiogenesis & Vasculature ⓘ

Hif1a↑, 2, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 1, GLUT1↑, 1, GLUT3↑, 5, GLUT4↑, 4,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, CRP↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 1, TNF-α↓, 2,

Cellular Microenvironment ⓘ

pH↝, 1,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 2, ChAT↑, 2, tau↓, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, eff↑, 1,

Clinical Biomarkers ⓘ

BMD↑, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 1,

Functional Outcomes ⓘ

cognitive↑, 2, hepatoP↑, 1, memory↑, 3, motorD↑, 1, neuroP↑, 5,
Total Targets: 71

Scientific Paper Hit Count for: GLUT3, GLUT3

3 Alpha-Lipoic-Acid
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Melatonin
1 Taurine

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#:928  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

GLUT3 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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