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⟱
2319- Api,    Apigenin sensitizes radiotherapy of mouse subcutaneous glioma through attenuations of cell stemness and DNA damage repair by inhibiting NF-κB/HIF-1α-mediated glycolysis
- in-vitro, GBM, NA
Glycolysis↓, Apigenin inhibited the activities of glycolytic enzymes and expressions of nuclear factor kappa B (NF-κB) p65, hypoxia inducible factor-lα (HIF-1α), glucose transporter (GLUT)-1/3 and pyruvate kinase isozyme type M2 (PKM2) proteins in tumor tissues.
NF-kB↓,
p65↓,
Hif1a↓,
GLUT1↓,
GLUT3↓,
PKM2↓,
RadioS↑, Apigenin sensitizes the radiotherapy of SU3-5R cells-inoculated subcutaneous glioma
TumVol↓, Moreover, the tumor weight and relative tumor weight in the three treatment groups were significantly lower than those in the control group
TumW↓,

2291- Ba,  BA,    Baicalein and Baicalin Promote Melanoma Apoptosis and Senescence via Metabolic Inhibition
- in-vitro, Melanoma, SK-MEL-28 - in-vitro, Melanoma, A375
LDHA↓, both baicalein and baicalin inhibited LDHα expression in Mel586, A375, and B16F0 melanoma cells, and ENO1 expression in SK-MEL-2 and A375 cells, as well as partially suppressed PKM2 expression in SK-MEL-2, A375, and B16F0 tumor cells
ENO1↓,
PKM2↓,
GLUT1↓, Baicalein and baicalin treatments markedly suppressed gene expression of Glut1, Glut3, HK2, TPI, GPI, and PFK1 in both human and mouse melanoma cells
GLUT3↓,
HK2↓,
PFK1↓,
GPI↓,
TPI↓,
GlucoseCon↓, baicalein and baicalin significantly inhibited glucose uptake abilities of four melanoma cell lines no matter of N-RAS and B-RAF mutation statuses
TumCG↓, baicalein and baicalin strongly suppressed tumor growth and proliferation of both human and mouse melanoma cells
TumCP↓,
mTORC1↓, Down-Regulation of mTORC1-HIF1α Signaling in Melanoma Cells Is Responsible for Glucose Metabolism Inhibition Induced by Baicalein and Baicalin
Hif1a↓,
Ki-67↓, We observed that baicalein and baicalin treatments markedly suppressed tumor cell proliferation as indicated by a decrease of Ki-67+ cell populations in tumor tissues

1640- CA,  MET,    Caffeic Acid Targets AMPK Signaling and Regulates Tricarboxylic Acid Cycle Anaplerosis while Metformin Downregulates HIF-1α-Induced Glycolytic Enzymes in Human Cervical Squamous Cell Carcinoma Lines
- in-vitro, Cerv, SiHa
GLS↓, downregulation of Glutaminase (GLS) and Malic Enzyme 1 (ME1)
NADPH↓, CA alone and co-treated with Met caused significant reduction of NADPH
ROS↑, increased ROS formation and enhanced cell death
TumCD↑,
AMPK↑, activation of AMPK
Hif1a↓, Met inhibited Hypoxia-inducible Factor 1 (HIF-1α). CA treatment at 100 μM for 24 h also inhibited HIF-1α
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓, PFKFB4
PKM2↓,
LDH↓,
cMyc↓, Met suppressed the expression of c-Myc, BAX and cyclin-D1 (CCND1) a
BAX↓,
cycD1/CCND1↓,
PDH↓, CA at a concentration of 100 µM caused inhibition of PDK activity
ROS↑, CA Regulates TCA Cycle Supply via Pyruvate Dehydrogenase Complex (PDH), Induces Mitochondrial ROS Generation and Evokes Apoptosis
Apoptosis↑,
eff↑, both drugs inhibited the expression of ACLY and FAS, but the greatest effect was detected after co-treatment
ACLY↓,
FASN↓,
Bcl-2↓,
Glycolysis↓, Met acts as a glycolytic inhibitor under normoxic and hypoxic conditions

946- Nimb,    Nimbolide retards T cell lymphoma progression by altering apoptosis, glucose metabolism, pH regulation, and ROS homeostasis
- in-vivo, NA, NA
Apoptosis↑,
Bcl-2↓,
P53↑, up-regulated expression of p53,
cl‑Casp3↑,
Cyt‑c↑,
ROS↑, induced ROS production by suppressing the expression of antioxidant regulatory enzymes, namely superoxide dismutase and catalase
SOD↓,
Catalase↓,
Glycolysis↓,
GLUT3↓,
LDHA↓, LDHA inhibitor
MCT1↓,
NHE1↓,
ATPase↓,
CAIX↓,

1231- PBG,    Caffeic acid phenethyl ester inhibits MDA-MB-231 cell proliferation in inflammatory microenvironment by suppressing glycolysis and lipid metabolism
- in-vitro, BC, MDA-MB-231
TumCP↓,
TumCMig↓,
TumCI↓,
MMP↓,
TLR4↓,
TNF-α↓,
NF-kB↓,
IL1β↓,
IL6↓,
IRAK4↓,
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓,
PKM2↓,
LDHA↓,
ACC↓,
FASN↓,
eff↓, After adding the glycolysis inhibitor 2-deoxy-D-glucose (2-DG), the inhibitory effects of CAPE on cell viability and migration were not significant when compared with the LPS group.

2419- SK,    Regulation of glycolysis and the Warburg effect in wound healing
- in-vivo, Nor, NA
Glycolysis↓, Treatment with 5–10 μM of the glycolysis inhibitor shikonin significantly decreased gene expression of the facilitative glucose transporters, GLUT1 and GLUT3
GLUT1↓,
GLUT3↓,
HK2↓, shikonin downregulated expression of the rate-limiting enzymes HK1 and HK2, although a 20 μM dose was needed
HK1↓, HK1
PFK1↓, Shikonin treatment also downregulated the rate-limiting enzyme PFK1
PFK2↓, PFK2 expression was only significantly lowered with a 20 μM dose
PKM2↓, 5 μM shikonin treatment inhibits gene expression of PKM2 (8.59 vs. 2.30, P < 0.001) and downregulated PDK1
lactateProd↓, coupled with decreased lactate production at higher concentrations of shikonin (10 μM and 20 μM)
GlucoseCon↓, shikonin effectively downregulated key enzymes involved in glucose uptake, glycolysis, and lactate production

2397- Wor,    Phytochemicals targeting glycolysis in colorectal cancer therapy: effects and mechanisms of action
- Review, Var, NA
lactateProd↓, Worenine-treated HCT116 and SW620 cells, the production of lactic acid and the uptake and consumption of glucose is significantly inhibited, the protein and mRNA levels of GLUT3, HK2, PFK-L, PKM2, and LDHA in HCT116 cells are reduced, and PKM activit
GlucoseCon↓,
GLUT3↓,
HK2↓,
PKM2↓,
LDHA↓,


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:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   HK1↓, 1,   ROS↑, 3,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ACLY↓, 1,   AMPK↑, 1,   CAIX↓, 1,   cMyc↓, 1,   ENO1↓, 1,   FASN↓, 2,   GLS↓, 1,   GlucoseCon↓, 3,   Glycolysis↓, 4,   GPI↓, 1,   HK2↓, 5,   lactateProd↓, 2,   LDH↓, 1,   LDHA↓, 4,   NADPH↓, 1,   PDH↓, 1,   PFK↓, 2,   PFK1↓, 2,   PFK2↓, 1,   PKM2↓, 6,   TPI↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↓, 1,   Bcl-2↓, 2,   cl‑Casp3↑, 1,   Cyt‑c↑, 1,   MCT1↓, 1,   TumCD↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTORC1↓, 1,   TumCG↓, 1,  

Migration ⓘ

ATPase↓, 1,   Ki-67↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 3,  

Barriers & Transport ⓘ

GLUT1↓, 5,   GLUT3↓, 7,   NHE1↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   IRAK4↓, 1,   NF-kB↓, 2,   p65↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,   TumW↓, 1,  
Total Targets: 62

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GLUT3, GLUT3
1 Apigenin (mainly Parsley)
1 Baicalein
1 Baicalin
1 Caffeic acid
1 Metformin
1 Nimbolide
1 Propolis -bee glue
1 Shikonin
1 Worenine
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#:1
  wNotes=on  sortOrder:rid,rpid

 

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