ALAT Cancer Research Results

ALAT, ALT, alanine aminotransferase: Click to Expand ⟱
Source:
Type: enzyme
(or ALT) -Used to be called serum glutamic-pyruvic transaminase (SGPT)
Most common in the liver.
An enzyme your body needs to break down proteins into energy.
It plays a crucial role in amino acid metabolism and is often measured in blood tests to assess liver function.
The catabolism of alanine by alanine aminotransferase 2 (ALT2) to pyruvate, was critical for the survival of non-small cell lung carcinoma (NSCLC) cells during glucose starvation. After knockdown of ALT2, cells were significantly more sensitive to glucose withdrawal compared to wildtype cells, which were rescued when supplemented with pyruvate.
Alanine aminotransferase (ALT) expression is highly elevated in the serum of patients with hepatocellular carcinoma.
A common example of dietary cancer therapy is the ketogenic diet, providing a fat-rich, low carbohydrate diet. The rationale is to reduce circulating glucose levels and induce ketosis.
Used as a clinical biomarker for Liver function.


Scientific Papers found: Click to Expand⟱
1415- HCA,    Hydroxycitrate delays early mortality in mice and promotes muscle regeneration while inducing a rich hepatic energetic status
- in-vivo, Nor, NA
*OS↑, mice treated with HC exhibited significant delays in spontaneous early mortality at 70%–90% mice survival in the longevity study
*toxicity↓, suggesting that chronic exposure to HC does not produce toxicity at the given dose
*AST∅, (AST) and ALT markers of liver damage were not altered
*ALAT∅,
*Strength↑, Remarkably, HC produced an increase in wire hang performance
*memory∅, HC did not produce remarkable effects in neurocognitive health and muscle strength in HFD‐fed mice
*other↑, HC promotes a rich energetic status in the liver
*other↑, HC potentiates muscle regeneration in vivo
*other↑, HC potentiates muscle regeneration in vivo

2903- LT,    Luteolin induces apoptosis by ROS/ER stress and mitochondrial dysfunction in gliomablastoma
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vivo, NA, NA
ER Stress↑, Luteolin induced a lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells by increasing intracellular reactive oxygen species (ROS) levels.
ROS↑,
PERK↑, Luteolin induced expression of ER stress-associated proteins, including phosphorylation of PERK, eIF2α, ATF4, CHOP and cleaved-caspase 12.
eIF2α↑,
ATF4↑,
CHOP↑,
Casp12↑,
eff↓, Inhibition of ROS production by anti-oxidant N-acetylcysteine could reverse luteolin-induced ER stress and mitochondrial pathways activation as well as apoptosis.
UPR↑, Researches indicate that abnormalities in ER function can cause ER stress, resulting in unfolded protein response (UPR),
MMP↓, integrity of mitochondrial membranes potential decreased in U87MG cells after treatment of 40 uM luteolin
Cyt‑c↑, release of cytochrome C to cytoplasm was elevated in U251MG cells
Bcl-2↓, significantly decreased the expression of anti-apoptotic protein Bcl-2 and increased the expression of pro-apoptotic protein Bax in U251MG and U87MG glioblastoms cells.
BAX↑,
TumCG↓, Luteolin inhibited tumor growth in a xenograft mouse model
Weight∅, luteolin did not affect body weight, alanine aminotransferase (ALT) or aspartate transaminase (AST)
ALAT∅,
AST∅,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT∅, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Casp12↑, 1,   Cyt‑c↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,   UPR↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Clinical Biomarkers ⓘ

ALAT∅, 1,   AST∅, 1,  

Functional Outcomes ⓘ

Weight∅, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

ALAT∅, 1,  

Transcription & Epigenetics ⓘ

other↑, 3,  

Clinical Biomarkers ⓘ

ALAT∅, 1,   AST∅, 1,  

Functional Outcomes ⓘ

memory∅, 1,   OS↑, 1,   Strength↑, 1,   toxicity↓, 1,  
Total Targets: 8

Scientific Paper Hit Count for: ALAT, ALT, alanine aminotransferase
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#:554  State#:%  Dir#:6
  wNotes=on  sortOrder:rid,rpid

 

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