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.
Scientific Papers found: Click to Expand⟱
7462- ,    Neuroprotective effects of honokiol: from chemistry to medicine
- Study, AD, NA
*ATR↑, Honokiol can permeate the blood brain barrier and the blood-cerebrospinal fluid to increase its bioavailability in neurological tissues.
*neuroP↑, Diverse studies have provided evidence on the neuroprotective effect of honokiol in the central nervous system, due to its potent antioxidant activity
*antiOx↑,
*Inflam↓, reduction in neuroinflammation
*Half-Life↝, rodent model [19]. The injection of 5–10 mg kg21 of honokiol has a plasma t1/2 value of 40–60 min, while the intraperitoneal injection in mice of 250 mg kg21 resulted in t1/2 value of 4–6 h, with a tmax of about 20–30 min
*ROS↓, fig 3
*Ca+2↓, demonstrated that honokiol counteracted Ab1–40 -induced elevation of Ca21, which is in strong agreement tothe antioxidative properties of honokiol
*GABA↓,
*COX2/PTGS2↓,
*memory↑, administration of ethanol extract of Magnolia officinalis (5 and 10 mg kg21 ) for 7 days improves the spatial long-term memory in scopolamine-induced mouse model of amnesia

4307- H2,    Hydrogen Gas Attenuates Toxic Metabolites and Oxidative Stress-Mediated Signaling to Inhibit Neurodegeneration and Enhance Memory in Alzheimer’s Disease Models
- in-vivo, AD, NA
*cognitive↑, H2 treatment significantly prevented cognitive deficits, oxidative stress, the accumulation of toxic metabolites, and the increase in inflammatory markers in 5xFAD mice.
*Inflam↓,
*ROS↓, H2 therapy has been shown to attenuate OS via selective reduction in ROS. 1.2-fold decrease in ROS levels
*neuroP↑, thereby reducing neurodegeneration and memory loss in AD.
*memory↑,
*BBB↑, making it easy for H2 to penetrate cell membranes and cross the blood–brain barrier
*BDNF↑, H2 therapy has been shown to modulate brain-derived neurotrophic factor and estrogen receptor β,
*TNF-α↓, We observed a significant reduction in TNF-α mRNA levels
*Catalase↑, 1.4-fold increase in catalase activity
*IL6↓, H2 treatment markedly suppressed TNF-α and IL-6 mRNA expression by 1.6-fold
*Aβ↓, observed that Aβ plaque accumulation in GFAP decreased by 2.8-fold in the cortex
*GABA↓, GABA levels were markedly lower
*Dose↝, Approximately 1–4% of H2 is deemed safe [ 36 ], and 3% of inhaled H2 has been reported to improve cognitive and diffusion tensor imaging scores in patients with AD

7484- H2,    Hydrogen Gas Attenuates Toxic Metabolites and Oxidative Stress-Mediated Signaling to Inhibit Neurodegeneration and Enhance Memory in Alzheimer's Disease Models
- in-vivo, AD, NA
*Dose↝, either 3% hydrogen gas (H2) or vehicle for 60 days.
*cognitive↑, H2 treatment significantly prevented cognitive deficits, oxidative stress, the accumulation of toxic metabolites, and the increase in inflammatory markers in 5xFAD mice.
*ROS↓, H2 treatment significantly attenuated ROS production in AβO-stimulated primary mouse astrocytes, showing a 1.2-fold reduction compared with vehicle
*Inflam↓, H2 Reduced OS and Decreased Neuroinflammation in AβO-Treated Astrocytes
*neuroP↑, H2 therapy can mitigate toxic metabolites in the astrocytic urea cycle, thereby reducing neurodegeneration and memory loss in AD.
*memory↑, H2 Inhalation Attenuates Memory Impairment in 5xFAD Mice
*Catalase↑, catalase activity increased by 20% following H2 treatment, although this increase was insignificant
*TNF-α↓, observed a significant reduction in TNF-α mRNA levels
*Aβ↓, Aβ plaque accumulation in GFAP decreased by 2.8-fold in the cortex
*GABA↓, GABA levels were markedly lower (p < 0.001) in the AβO-induced astrocytes treated with H2 than in those treated with vehicle
*H2O2↓, H2 treatment attenuated toxic metabolite accumulation, including Aβ, H2O2, and GABA, which were markedly reduced after H2
*GFAP↓, These suggest that astrocyte function was enhanced after H2 treatment due to reduced astrogliosis, denoted by the decrease in the GFAP level.
*antiOx↑, The antioxidant defense system is key to H2’s efficacy, which is modulated upstream by nuclear factor erythroid 2-related factor 2 (Nrf2)
*NRF2↑,

7068- VitD3,    Vitamin D Reduces GABA-Positive Astrocytes in the 5xFAD Mouse Model of Alzheimer’s Disease
- in-vivo, AD, NA
*Aβ↓, vitamin D supplementation ameliorated these effects, leading to a reduction in Aβ plaques and GABA-positive astrocytes.
*GABA↓,
Risk↓, We demonstrated that vitamin D deficiency could increase the production of Aβ in an AD mouse model, while upregulating genes involved in Aβ synthesis and downregulating genes involved in Aβ degradation


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:


Functional Outcomes(tgid=23) ⓘ

Risk↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

GFAP↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 2,   H2O2↓, 1,   NRF2↑, 1,   ROS↓, 3,  

DNA Damage & Repair(tgid=10) ⓘ

ATR↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL6↓, 1,   Inflam↓, 3,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,   GABA↓, 4,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 2,   memory↑, 3,   neuroP↑, 3,  
Total Targets: 22

Scientific Paper Hit Count for: GABA, γ-aminobutyric acid
2 Hydrogen Gas
1 Vitamin D3
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#:1205  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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