ALDOA Cancer Research Results

ALDOA, Aldolase A: Click to Expand ⟱
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ALDOA (Aldolase A) is an enzyme involved in glycolysis, the metabolic pathway that converts glucose into energy.
Expression level of ALDOA was significantly related to the prognosis of brain cancer, skin cancer, lung adenocarcinoma and breast cancer.
Aldolase enzymes, particularly ALDOA, ALDOB, and ALDOC, play a crucial role in the development and progression of cancer. While the aldolase family is mainly known for its involvement in the glycolysis pathway, these enzymes also have various pathological and physiological functions through distinct signaling pathways such as Wnt/β-catenin, EGFR/MAPK, Akt, and HIF-1α. ALDOA (Aldolase A) is an enzyme involved in glycolysis, the metabolic pathway that converts glucose into energy.
ALDOA is often overrepresented and has been associated with poor prognosis in various malignancies. Its expression levels can serve as potential biomarkers for tumor aggressiveness and patient outcomes.
Scientific Papers found: Click to Expand⟱
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

2289- Ba,  Rad,    Baicalein Inhibits the Progression and Promotes Radiosensitivity of Esophageal Squamous Cell Carcinoma by Targeting HIF-1A
- in-vitro, ESCC, KYSE150
TumCP↓, Radiation combined with baicalein could significantly inhibit the proliferation and migration of esophageal cancer cells compared with that of 6 Gy rays alone
TumCMig↓,
Glycolysis↓, 20μM baicalein reduced glycolysis in KYSE150 cells
cycD1/CCND1↓,
CDK4↓,
ECAR↓, Baicalein reduces ECAR and glycoPER
TumCCA↑, baicalein arrested cells in the G1 phase of the cell cycle
HK1↓, HK1 (4QS9),13 ALDH2, GPI and ALDOA are the key enzymes in the process of glycolysis.
ALDH↓,
ALDOA↓,
PKM2↓, protein levels of HIF-1A and PKM2 decreased significantly after baicalein treatment.
Hif1a↓,

933- CUR,  EP,    Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study
- in-vitro, BC, NA
Apoptosis↑,
ALDOA↓,
ENO2↓,
LDHA↓, LDH inhibitor
LDHB↓,
PFKP↓,
PGK1↓,
PGM1↓,
PGAM1↓,
OXPHOS↑, upregulation of 10 oxidative phosphorylation pathway proteins
TCA↑, upregulation of 8 tricarboxylic acid (TCA) cycle proteins

7761- ISL,    Targeting digestive system cancers with isoliquiritigenin: a comprehensive review of antitumor mechanisms
- Review, Var, NA
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.


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   HK1↓, 2,   i-Iron↑, 1,   OXPHOS↓, 1,   OXPHOS↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALDOA↓, 4,   ECAR↓, 1,   ENO1↓, 2,   ENO2↓, 1,   Glycolysis↓, 3,   HK2↓, 1,   lactateProd↓, 2,   LDHA↓, 2,   LDHB↓, 1,   MCT4↓, 1,   NADPH↓, 1,   PFKP↓, 1,   PGAM1↓, 1,   PGK1↓, 2,   PGM1↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 1,   PPP↓, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   Ferroptosis↑, 1,   JNK↑, 1,   p27/CDKN1B↑, 1,   p38↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

GRP78/BiP↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ALDH↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↑, 1,  

Migration(tgid=13) ⓘ

TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   GLUT4↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IκB↑, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↓, 1,   eff↑, 1,   Half-Life↓, 1,   RadioS↑, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ALDOA, Aldolase A
1 Apigenin (mainly Parsley)
1 Baicalein
1 Radiotherapy/Radiation
1 Curcumin
1 Electrical Pulses
1 Isoliquiritigenin
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#:567  State#:%  Dir#:1
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