HK1 Cancer Research Results

HK1, Hexokinase 1: Click to Expand ⟱
Source:
Type:
Accelerated glucose metabolism is a common feature of cancer cells. Hexokinases catalyze the first committed step of glucose metabolism. HK1 (Hexokinase 1) is a key enzyme in glycolysis, catalyzing the phosphorylation of glucose to glucose-6-phosphate. It is critical for maintaining cellular energy homeostasis and is part of the metabolic reprogramming often observed in cancer cells.

• In some tumors, HK1 is upregulated to meet the high glycolytic demands of rapidly proliferating cancer cells. However, the expression pattern can be context-dependent, with some cancers potentially showing moderate or variable HK1 levels compared to the normal tissue counterpart.

• Enhanced HK1 expression supports the high glycolytic flux commonly seen in cancers (the Warburg effect), facilitating anabolic processes and thereby aiding in rapid cell proliferation and biomass accumulation.

• Changes in HK1 expression can also alter the balance between glycolysis and oxidative phosphorylation, potentially impacting reactive oxygen species (ROS) production and cellular redox status in tumors.
Scientific Papers found: Click to Expand⟱
2424- 2DG,  SRF,    The combination of the glycolysis inhibitor 2-DG and sorafenib can be effective against sorafenib-tolerant persister cancer cells
- in-vitro, HCC, Hep3B - in-vitro, HCC, HUH7
ChemoSen↓, combination of 2-DG and sorafenib reduced persister tumor growth in mice
Glycolysis↓, The glycolysis inhibitor 2-Deoxy-D-glucose (2-DG), an inhibitor of all forms of HK
HK1↓,
HK2↓,
ATP↓, reducing ATP production

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↓,

2457- MET,    Metformin Impairs Glucose Consumption and Survival in Calu-1 Cells by Direct Inhibition of Hexokinase-II
- in-vitro, Lung, Calu-1
HK1↓, Here we show that metformin impairs the enzymatic function of HKI and II in Calu-1 cells.
HK2↓,
GlucoseCon↓, This inhibition virtually abolishes cell glucose uptake
MMP↓, results in mitochondrial depolarization and subsequent cell death
ATP↓, Metformin effects resulted in a marked and dose-dependent increase in the AMP/ATP ratio

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


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 ⓘ

HK1↓, 5,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 3,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 2,   ECAR↓, 1,   ENO1↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 4,   HK2↓, 4,   lactateProd↓, 2,   NADPH↓, 1,   PFK1↓, 1,   PFK2↓, 1,   PGK1↓, 1,   PI3K/Akt↓, 1,   PKM2↓, 2,   PPP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp9↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,  

Migration ⓘ

TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,   GLUT3↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   eff↓, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: HK1, Hexokinase 1
1 2-DeoxyGlucose
1 Sorafenib (brand name Nexavar)
1 Apigenin (mainly Parsley)
1 Baicalein
1 Radiotherapy/Radiation
1 Metformin
1 Shikonin
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#:448  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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