ENO1 Cancer Research Results

ENO1, α-Enolase: Click to Expand ⟱
Source:
Type:
Also known as 2-phospho-D-glycerate hydrolase
Is a glycolytic enzyme that catalyzes the conversion of 2-phosphoglyceric acid to phosphoenolpyruvic acid during glycolysis.
ENO1's glycolytic function deregulates cellular energetic, sustains tumor proliferation, and inhibits cancer cell apoptosis. Moreover, ENO1 evades growth suppressors and helps tumors to avoid immune destruction. Besides, ENO1 “moonlights” on the cell surface and acts as a plasminogen receptor, promoting cancer invasion and metastasis by inducing angiogenesis. Overexpression of ENO1 on a myriad of cancer types together with its localization on the tumor surface makes it a great prognostic and diagnostic cancer biomarker as well as an accessible oncotherapeutic target.
Scientific Papers found: Click to Expand⟱
5165- AL,    The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects
- in-vitro, AML, Jurkat - in-vitro, Nor, L929
necrosis↑, Allicin induces apoptosis or necrosis in a dose-dependent manner but biocompatible doses influence cellular metabolism and signalling cascades.
Thiols↓, Oxidation of protein thiols and depletion of the glutathione pool are thought to be responsible for allicin's physiological effects.
GSH↓,
ENO1↓, allicin caused inhibition of enolase activity, an enzyme considered a cancer therapy target.
Zn2+↑, Allicin leads to Zn2+ release in murine EL-4 cells
Glycolysis↓, suggests that allicin can inhibit glycolysis which provides electron donors for ATP generation required for cellular biosynthesis pathways and growth of the cells.
ATP↓,
BioAv↓, achieving therapeutically relevant concentrations of allicin via the oral route is therefore unlikely and more direct routes of application to the desired site of action need to be considered

206- Api,    Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, Melanoma, A375 - in-vitro, Lung, H2030 - in-vitro, CRC, SW480
Glycolysis↓, glucose consumption, lactate production, and ATP production were all strongly decreased by apigenin
lactateProd↓,
PGK1↓,
ALDOA↓,
GLUT1↓, Apigenin reduces GLUT1 expression levels.
ENO1↓,
ATP↓,
Casp9↑,
Casp3↑,
cl‑PARP↑, cleavage
PI3K/Akt↓,
HK1↓, HK1, HK2
HK2↓,
ROS↑, Apigenin causes oxidative stress leading to apoptosis. Because apoptotic signal transduction cascades involving caspase-9, -3 and PARP cleavage can be activated by increased ROS levels
Apoptosis↑,
eff↓, Cancer cells expressing high levels of GLUT1 are resistant to apigenin-induced apoptosis through metabolic compensation of glucose utilization.
NADPH↓, apigenin significantly decreased glucose utilization through suppression of GLUT1 expression, and consequently decreased NADPH production, which led to increased ROS levels.
PPP↓, inhibition of the PPP

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

2826- FIS,    Fisetin induces apoptosis in breast cancer MDA-MB-453 cells through degradation of HER2/neu and via the PI3K/Akt pathway
- in-vitro, BC, MDA-MB-453
Apoptosis↑, fisetin induced apoptosis of these cells by various mechanisms, such as inactivation of the receptor, induction of proteasomal degradation, decreasing its half-life, decreasing enolase phosphorylation, and alteration of PI3K/AKT
p‑ENO1↓,
DNAdam↑, displaying DNA fragmentation pattern
PI3K↑, Fisetin increased PI3K activity at 10 uM, which gradually declines on treatment with higher concentrations (25 or 50 uM)
p‑Akt↑, Fisetin (10 uM) increased phosphorylation of Akt in MDA-MB-453 cells greater than control. Higher concentrations of fisetin (25 or 50 uM) gradually decreased the phosphorylation of Akt.
HER2/EBBR2↓, fisetin induced HER2 depletion

2178- itraC,    Itraconazole inhibits tumor growth via CEBPB-mediated glycolysis in colorectal cancer
- in-vivo, CRC, HCT116
TumCG↓, We found that itraconazole could inhibit tumor growth and glycolysis
Glycolysis↓, itraconazole could repress CRC tumor growth by inhibiting glycolysis
CEBPB?, CEBPB was a new target for itraconazole, and that silencing CEBPB could repress CRC glycolysis and tumor growth by inhibiting ENO1 expression
ENO1↓, glycolysis enzymes (ENO1, LDHA, PGK1, PKM and GAPDH) was significantly decreased after itraconazole treatment
LDHA↓,
PKM2↓,
GAPDH↓,
ECAR↓, itraconazole treatment could significantly reduce ECAR and OCR
OCR↓,


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   HK1↓, 1,   ROS↑, 1,   Thiols↓, 1,  

Metal & Cofactor Biology ⓘ

Zn2+↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   ECAR↓, 1,   ENO1↓, 4,   p‑ENO1↓, 1,   GAPDH↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   GPI↓, 1,   HK2↓, 2,   lactateProd↓, 1,   LDHA↓, 2,   NADPH↓, 1,   PFK1↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 2,   PPP↓, 1,   TPI↓, 1,  

Cell Death ⓘ

p‑Akt↑, 1,   Apoptosis↑, 2,   Casp3↑, 1,   Casp9↑, 1,   necrosis↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CEBPB?, 1,   mTORC1↓, 1,   PI3K↑, 1,   TumCG↓, 2,   Zn2+↑, 1,  

Migration ⓘ

Ki-67↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,   GLUT3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   eff↓, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   Ki-67↓, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ENO1, α-Enolase
1 Allicin (mainly Garlic)
1 Apigenin (mainly Parsley)
1 Baicalein
1 Baicalin
1 Fisetin
1 itraconazole
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#:568  State#:%  Dir#:1
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