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⟱
3441- ALA,    α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice
- in-vivo, AD, NA
*tau↓, α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research
*GlucoseCon↑, chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brain
*GLUT3↑,
*GLUT4↑,
*VEGF↑,
*HO-1↑,
*Glycolysis↑, LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1).
*HK1↑, Our results indicated that the activity of HK was significantly increased after 10 mg/kg LA treatment.
*PGC-1α↑,
*Hif1a↑, found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.
*neuroP↑,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

HK1↑, 1,   HO-1↑, 1,  

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↑, 1,   Glycolysis↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

GLUT3↑, 1,   GLUT4↑, 1,  

Synaptic & Neurotransmission ⓘ

tau↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 11

Scientific Paper Hit Count for: HK1, Hexokinase 1
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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