GABA Cancer Research Results

GABA, γ-aminobutyric acid: Click to Expand ⟱

Source:

Type:

– Some studies have reported upregulated expression of certain GABA receptor subunits (e.g., GABA_A receptor subunits) in breast tumors.

– Increased expression has been associated with enhanced cell proliferation and migration, with some reports linking this to a poorer prognosis.
-GABAergic transmission is deficient in anxiety. -Neurons expressing GABAA α1 receptors can mediate sedation, -while those expressing GABAA α2 receptors mediate anxiolytic. -In addition, extra-synaptic GABAA α5 receptors can also regulate the activity of hippocampal pyramidal cells, thereby affecting associative temporal and spatial memory

Gamma-aminobutyric acid — Gamma-aminobutyric acid is an endogenous non-protein amino acid, inhibitory neurotransmitter, metabolic intermediate, and signaling ligand commonly abbreviated GABA. As a database target, it represents changes in GABA concentration, synthesis, secretion, uptake, extracellular accumulation, or GABA-shunt utilization rather than modulation of a specific GABA receptor. GABA is synthesized from glutamate by GAD1/GAD67 and GAD2/GAD65, transported by GABA transporters, and metabolized primarily by ABAT/GABA transaminase. In cancer, GABA may be produced by tumor, neural, stromal, or immune cells and can influence proliferation, invasion, mitochondrial metabolism, β-catenin signaling, and antitumor immunity. Its biological direction is strongly tumor-, receptor-, concentration-, and compartment-dependent.

Typical cancer modulation: Variable/context-dependent. GABA production, secretion, extracellular accumulation, uptake, or GABA-shunt utilization may be ↑ in tumors that exploit GABA for metabolic adaptation, β-catenin activation, growth, invasion, or immune evasion. GABA signaling may instead suppress proliferation or migration in tumors expressing inhibitory GABA receptor configurations.

Normal-cell relevance: GABA generally reduces neuronal excitability through GABA receptor signaling and also regulates pancreatic, immune, gastrointestinal, vascular, and endocrine functions. In Alzheimer’s disease, reduced phasic inhibition and excessive astrocyte-derived tonic GABA may coexist in different circuits; therefore total GABA direction alone may not indicate whether GABAergic function is beneficial or pathological.

Target classification: Neurotransmitter; amino-acid metabolite; signaling ligand; tumor-microenvironment mediator; metabolic substrate.

NA, Not Available: Click to Expand ⟱

none (reserved)

Scientific Papers found: Click to Expand⟱

1892-

MGO,

Role of Glyoxalase 1 (Glo1) and methylglyoxal (MG) in behavior: recent advances and mechanistic insights

Review,

NA,

MGO↑, ROS↑, other↝, GABA↑, other∅,

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:

Redox & Oxidative Stress(tgid=1) ⓘ

MGO↑, 1, ROS↑, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1, other∅, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

GABA↑, 1,
Total Targets: 5

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: GABA, γ-aminobutyric acid

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