GLUT4 Cancer Research Results
GLUT4, Glucose Transporter 4: Click to Expand ⟱
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GLUT4 (Glucose Transporter 4) is a protein that plays a crucial role in glucose metabolism by facilitating the transport of glucose across cell membranes. GLUT4 is a member of the facilitated glucose transporter family and is primarily expressed in adipose tissue and skeletal muscle.
GLUT4 has been shown to be overexpressed in many types of tumors, and its expression has been linked to cancer cell growth, survival, and metastasis.
GLUT4 is involved in the regulation of glucose metabolism in cancer cells, and its overexpression has been shown to promote glucose uptake and energy production in cancer cells.
GLUT4 promotes glucose uptake and energy production in cancer cells.
GLUT4 expression is linked to poor prognosis in various types of cancer.
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Scientific Papers found: Click to Expand⟱
*CEBPA↓, Figure 2
*PPARγ↓,
*FASN↓,
*SREBP1/SREBF1↓,
*FABP4↓,
*GLUT4↓,
*β-catenin/ZEB1↑, Boron Activated the β-Catenin Signaling Pathway
*MMP2↓, As shown in Fig. 6, soluble transforming growth factor receptor 1 (sTNFR1) and matrix metalloproteinase 2
(MMP2) protein levels decreased in the presence of boron
*FGF↑, whereas basic fibroblast growth factor expression (bFGF) increased
*Ca+2?, Boric acid has been reported to interact with NAD + and inhibit cyclic ADP ribose-activated Ca 2+ release from ryanodine receptor, leading to decreased endoplasmic reticulum luminal Ca 2+ concentrations
mitA↑, FBZ destabilizes microtubules, critical for cell division, leading to mitotic arrest and apoptosis.
Apoptosis↑,
GLUT4↓, FBZ inhibits glucose uptake by downregulating GLUT transporters and hexokinase II, starving cancer cells reliant on aerobic glycolysis (Warburg effect).
HK2↓,
Warburg↓,
TumCCA↑, FBZ induces G2/M phase arrest and promotes apoptosis via p53 activation and caspase activation.
P53↑,
Casp↑,
TumCP↓, confirmed dose-dependent proliferation inhibition and apoptosis.
ROS↑, FBZ induces reactive oxygen species (ROS) accumulation, enhancing ferroptosis and apoptosis, particularly in 5-fluorouracil-resistant colorectal cancer cells.
Ferroptosis↑,
TumVol↓, A549 lung cancer xenografts in nude mice, reported significant tumor shrinkage with oral FBZ administration (1 mg/mouse every 2 days for 12 days).
Dose↝, The case of Joe Tippens, who reported complete remission from stage IV small-cell lung cancer after taking FBZ (222 mg daily) alongside vitamin E, CBD oil, and curcumin, has fueled public interest.
BioAv↓, FBZ’s poor water solubility and low systemic bioavailability limit its ability to reach therapeutic levels in tumors when administered orally.
RadioS↝, Given preclinical evidence of synergy with radiation or docetaxel, trials should explore FBZ’s role as an adjunct to conventional treatments, potentially enhancing efficacy in resistant cancers.
ChemoSen↑,
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vitro+vivo, |
Lung, |
A549 |
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in-vitro, |
Lung, |
H460 |
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TumCD↑, exerts cytotoxicity to human cancer cells at micromolar concentrations.
P53↑, Simultaneously, it caused mitochondrial translocation of p53 and effectively inhibited glucose uptake, expression of GLUT transporters as well as hexokinase (HK II) - a key glycolytic enzyme that most cancer cells thrive on.
GlucoseCon↓,
GLUT4↓, FZ exposure reduced the expression of Glut-4 transporter as well as hexokinase (HK II), which may be linked to p53 activation and alteration of microtubule dynamics
HK2↓,
TumCG↓, It blocked the growth of human xenografts in nu/nu mice model when mice were fed with the drug orally.
P-gp/ABCB1∅, treated and untreated cells showed comparable levels of Rho123 accumulation affirming that FZ is not a substrate or inhibitor of P-gp.
TumCCA↑, FZ treatment results in early G2/M block accompanied by cell death
CycB/CCNB1↓, simultaneous decrease in cyclin B1 levels
eff↑, Tumour cell lines with wild-type p53 show enhanced sensitivity to FZ induced apoptosis
selectivity↑, Remarkably, FZ showed less toxicity towards primary epithelial cells cultured from rat lung tissue as compared to a lung cancer cell line
MMP↓, Correspondingly, mitochondrial membrane depolarization
lactateProd↓, FZ treatment also resulted in reduced lactate levels (Fig. 8c). Hence, FZ induced cell death appeared to be related to inhibition of glucose uptake.
eff↑, we conclude that FZ shows synergistic effect with DCA, 2DG and over a range of doses with taxol.
Dose↝, A549 cells and mice bearing tumours (2–3 mm) were fed with FZ (1 mg/mouse) orally every second day for 12 days
TumCG↓, FZ inhibits tumour cell growth in vivo by inducing apoptosis of tumour cells.
angioG↓, Ginsenoside Rg3 inhibits angiogenesis in gastric precancerous lesions through downregulation of Glut1 and Glut4
GLUT1↓,
GLUT4↓,
Hif1a↓, PCa downregulation of HIF-1α, GLUT1, GLUT4, HK2 and LDHA; decreased cell motility and invasion by downregulating MUC4
GLUT1↓,
GLUT4↓,
HK2↓,
LDHA↓,
MUC4↓,
TumCCA↑, Hematological malignancies, cell cycle arrest, loss of MMP
MMP↓,
NF-kB↓, graviola treatment suppresses nuclear factor-κB (NF-κB) signaling, induces reactive oxygen species (ROS) production and increases the Bax/Bcl-2 ratio–mediated attenuation of mitochondrial membrane potential (MMP), cytosolic cytochrome c and caspase-3
ROS↓,
Bax:Bcl2↑,
ER(estro)↓, graviola inhibited the growth of MCF-7 breast cancer cells by decreasing estrogen receptor (ER), cyclin D1 and antiapoptotic gene Bcl2 expression in cell lines and xenografts
cycD1/CCND1↓,
chemoPv↑, Graviola extracts have also been used as chemopreventive agent in many carcinogen-induced mouse models
hepatoP↑, Annona muricata is commonly used to treat several liver disorders, particularly jaundice.
GlucoseCon↓, decreased glucose absorption
ATP↓,
HIF-1↓,
GLUT1↓,
GLUT4↓,
HK2↓,
LDHA↓,
ERK↓,
Akt↓,
Apoptosis↑,
NF-kB↓,
ROS↑, increases ROS production
Bax:Bcl2↑,
MMP↓,
Casp3↑,
Casp9↑,
p‑JNK↓,
Hif1a↓,
NF-kB↓,
GLUT1↓,
GLUT4↓,
HK2↓,
LDHA↓,
TumCCA↑, G0/G1 cell cycle arrest
TumMeta↓,
GlucoseCon↓, 5%-20% of control for glucose uptake
ATP↓,
necrosis↑, cells incubated with Graviola extract have a gain in cell volume, a characteristic of necrotic cell death
Casp∅, Caspase-3 expression values remained statistically unaltered by treatment with the extract, suggesting that apoptotic pathways are not involved
p‑FAK↓,
MMP9↓,
MUC4↓, significant downregulation in MUC4
EGFR↓,
PI3K/Akt↓,
NF-kB↓,
JAK↓,
STAT↓,
Hif1a↓, inhibition of HIF-1α, GLUT1, and GLUT4 [
GLUT1↓,
GLUT4↓,
ROS↑, generation of reactive oxygen species (ROS) via upregulatoin of enzyme systems like catalase (CAT), superoxide dismutase (SOD), and heme-oxygenase (HO-1) expression
Catalase↑,
SOD↑,
HO-1↑,
EGFR↓,
cycD1/CCND1↓,
Bcl-2↓,
TumCCA↑, G1 cell cycle arrest, 2nd ref :G0/G1 phase cell arrest
Apoptosis↑,
ROS↑,
MMP↓,
BAX↑,
Cyt‑c↑, cytochrome c release
Hif1a↓,
NF-kB↓,
GLUT1↓,
GLUT4↓,
HK2↓,
LDHA↓,
ATP↓,
JAK↓, ISL exerts significant anti-ovarian cancer effects through multitarget regulation of the JAK/STAT pathway.
STAT↓,
toxicity↓, With the advantages of low toxicity and multi-pathway modulation, ISL is a promising natural candidate for targeted therapy,
*antiOx↑, exhibits significant antioxidant capacity, effectively scavenging free radicals and reducing oxidative stress-induced cellular damage
*ROS↓,
*NRF2↑, By activating the Nrf2/ARE signaling pathway, ISL induces the expression of antioxidant enzymes such as HO-1 and NQO1, thereby enhancing cellular antioxidant defense systems
*ARE↑,
*HO-1↑,
*NQO1↑,
*Inflam↓, Regarding anti-inflammatory effects, ISL suppresses NF-κB and MAPK signaling pathways, reducing inflammatory factor production and alleviating inflammatory responses
*NF-kB↓,
*MAPK↓,
*SOD↑, it maintains intracellular antioxidant defense mechanisms, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity to mitigate oxidative stress-induced cellular damage
*Catalase↑,
*GPx↑,
*AntiViral↑, Its antiviral activity manifests as ISL’s ability to disrupt viral replication cycles, inhibit viral protein synthesis, and suppress multiple viruses.
*NADPH↑, ISL reduces ROS production by activating the Nrf2 pathway or upregulating NADPH oxidase expression and activity
ROS↓, In SK-MEL-28 melanoma cells, ROS inhibition suppressed p38α (Thr180/Tyr182) phosphorylation, blocked the p38-mTOR-STAT3 (Ser727) cascade. This leads to decreased STAT3 transcriptional activity, silencing downstream cyclin D1 and survivin expression,
p38↓,
mTOR↓,
STAT3↓,
cycD1/CCND1↓,
survivin↓,
p38↑, ISL inhibits autophagy flux in pancreatic cancer cells by activating the p38-MAPK signaling pathway,
MAPK↑,
mtDam↑, This mechanism disrupts cellular clearance of damaged mitochondria, triggers endoplasmic reticulum stress and oxidative stress, ultimately inducing apoptosis.
ER Stress↑,
ROS↑,
Apoptosis↑,
GLUT4↓, chemically synthesized derivative ISL-17 in MKN45 gastric cancer cells interferes with energy metabolism (Warburg effect) by inhibiting GLUT4-mediated glucose uptake, leading to decreased ATP levels and increased ROS accumulation.
ATP↓,
Glycolysis↓, This process triggers an energy crisis by blocking glycolysis and oxidative phosphorylation, further enhancing the cytotoxic effects of ROS and thereby inhibiting tumor growth
eff↑, Combining ISL with mTOR inhibitors significantly enhances growth inhibition of ovarian cancer cells by dual blockade of the PI3K/Akt/mTOR pathway
Apoptosis↑, via the regulation of apoptosis, autophagy, cell cycle arrest, redox homeostasis, and tumor microenvironment (TME) remodeling.
TumAuto↑,
TumCCA↑,
ROS↑, ROS ↑, JNK ↑, p38 ↑, ERK ↓, STAT3 ↓, NF-κB ↓, IκB ↑, Bcl-2 ↓, Bax ↑, Cleaved caspase-3 ↑, Cleaved PARP ↑, p21 ↑, p27 ↓, Cyclin B1 ↓, CDK1/2 ↓
JNK↑,
p38↑,
STAT3↑,
NF-kB↓,
IκB↑,
Bcl-2↓,
BAX↑,
cl‑Casp3↑,
cl‑PARP↑,
P21↑,
p27/CDKN1B↑,
CycB/CCNB1↑,
CDK1↓,
CDK2↓,
GRP78/BiP↓, ISL also modulates the TME by downregulating GRP78 and inhibiting the PI3K/AKT/mTOR signaling pathway, thereby promoting apoptosis and autophagy
PI3K↓,
Akt↓,
mTOR↓,
eff↑, ISL-17 is a newly synthesized analog of ISL designed to improve its pharmacological properties.
GLUT4↓, ISL inhibits GLUT4-mediated glucose uptake, reduces lactate production and secretion, and suppresses both mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis.
lactateProd↓,
OXPHOS↓,
Glycolysis↓,
BioAv↑, ISL-loaded nanoliposomes represent a novel drug delivery system with excellent self-assembly and biocompatibility properties.
ENO1↓, ISL nanoliposomes suppress the expression of key glycolytic enzymes including Enolase 1 (ENO1), Aldolase A (ALDOA), lactate dehydrogenase A (LDHA), and monocarboxylate transporter 4 (MCT4).
ALDOA↓,
LDHA↓,
MCT4↓,
RadioS↑, ISL also enhances the radiosensitivity of HCC cells by modulating oxidative stress pathways.
Ferroptosis↑, ISL promotes ferroptosis by modulating iron metabolism and enhancing oxidative stress.
i-Iron↑, ISL treatment significantly elevated intracellular ferrous ion (Fe2+) levels, along with a marked increase in ROS and lipid peroxidation.
BioAv↑, Optimization of ISL delivery via two advanced nanocarrier systems has significantly addressed its poor aqueous solubility and limited bioavailability.
Half-Life↓, Furthermore, like many flavonoids, ISL suffers from poor oral bioavailability and rapid metabolic clearance.
TumCG↓,
LC3II↑,
p62↓,
ATP↓,
Pyruv↓,
GlucoseCon↑, promoted glucose uptake
HK2↓,
PFK1↓,
GLUT4↓,
Glycolysis↓,
JAK2↓,
p‑STAT3↓,
p‑STAT5↓,
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 1, Ferroptosis↑, 2, HO-1↑, 1, i-Iron↑, 1, OXPHOS↓, 1, ROS↓, 2, ROS↑, 6, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 5, MMP↓, 4, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALDOA↓, 1, ENO1↓, 1, GlucoseCon↓, 3, GlucoseCon↑, 1, Glycolysis↓, 3, HK2↓, 7, lactateProd↓, 2, LDHA↓, 5, MCT4↓, 1, PFK1↓, 1, PI3K/Akt↓, 1, Pyruv↓, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Apoptosis↑, 5, BAX↑, 2, Bax:Bcl2↑, 2, Bcl-2↓, 2, Casp↑, 1, Casp∅, 1, Casp3↑, 1, cl‑Casp3↑, 1, Casp9↑, 1, Cyt‑c↑, 1, Ferroptosis↑, 2, JNK↑, 1, p‑JNK↓, 1, MAPK↑, 1, necrosis↑, 1, p27/CDKN1B↑, 1, p38↓, 1, p38↑, 2, survivin↓, 1, TumCD↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, GRP78/BiP↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3II↑, 1, p62↓, 1, TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↑, 2, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 1, CycB/CCNB1↓, 1, CycB/CCNB1↑, 1, cycD1/CCND1↓, 3, mitA↑, 1, P21↑, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, mTOR↓, 2, PI3K↓, 1, STAT↓, 2, STAT3↓, 1, STAT3↑, 1, p‑STAT3↓, 1, p‑STAT5↓, 1, TumCG↓, 3,
Migration(tgid=13) ⓘ
p‑FAK↓, 1, MMP9↓, 1, MUC4↓, 2, TumCP↓, 1, TumMeta↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, EGFR↓, 2, HIF-1↓, 1, Hif1a↓, 4,
Barriers & Transport(tgid=15) ⓘ
GLUT1↓, 6, GLUT4↓, 11, P-gp/ABCB1∅, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IκB↑, 1, JAK↓, 2, JAK2↓, 1, NF-kB↓, 6,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
ER(estro)↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 2, ChemoSen↑, 1, Dose↝, 2, eff↑, 4, Half-Life↓, 1, RadioS↑, 1, RadioS↝, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 2,
Functional Outcomes(tgid=23) ⓘ
chemoPv↑, 1, hepatoP↑, 1, toxicity↓, 1, TumVol↓, 1,
Total Targets: 100
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, ARE↑, 1, Catalase↑, 1, GPx↑, 1, HO-1↑, 1, NQO1↑, 1, NRF2↑, 1, ROS↓, 1, SOD↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
FABP4↓, 1, FASN↓, 1, NADPH↑, 1, PPARγ↓, 1, SREBP1/SREBF1↓, 1,
Cell Death(tgid=5) ⓘ
MAPK↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CEBPA↓, 1, FGF↑, 1,
Migration(tgid=13) ⓘ
Ca+2?, 1, MMP2↓, 1, β-catenin/ZEB1↑, 1,
Barriers & Transport(tgid=15) ⓘ
GLUT4↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 1, NF-kB↓, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1,
Total Targets: 24
Scientific Paper Hit Count for: GLUT4, Glucose Transporter 4
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
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