ARG Cancer Research Results

ARG, Arginine: Click to Expand ⟱
Source:
Type:

Arginine is a semi-essential amino acid involved in protein synthesis, nitric oxide production, the urea cycle, creatine synthesis, polyamine production, immune-cell function, and cellular metabolism. Its availability is regulated partly by arginase-1 (ARG1), arginase-2 (ARG2), nitric oxide synthases, and enzymes involved in arginine synthesis and recycling.
-higher ARG1/ARG2 activity → lower available arginine

In cancer, arginine has context-dependent effects. Some tumours are dependent on extracellular arginine because they have reduced expression of argininosuccinate synthetase 1 (ASS1) or other arginine-synthesis enzymes. Arginine depletion may therefore inhibit the growth of arginine-auxotrophic tumours. In contrast, adequate arginine can support T-cell proliferation, cytotoxic activity, and antitumour immune responses. Increased ARG1 or ARG2 activity may deplete arginine in the tumour microenvironment and suppress T-cell function.

In neurodegenerative disease, arginine metabolism influences nitric oxide production, vascular function, mitochondrial activity, oxidative stress, and neuroinflammation. Excessive arginase activity may reduce arginine availability for nitric oxide synthase, while dysregulated nitric oxide production may contribute to oxidative and nitrosative stress.

Direction: context-dependent. Increased arginine availability may support immune and vascular function, whereas arginine depletion may be beneficial in arginine-dependent tumours. Arginine is a direction-neutral metabolite target, with the favourable direction recorded at the individual study or disease-context level.



Scientific Papers found: Click to Expand⟱
6692- DFC,    Diclofenac Inhibits Tumor Growth in a Murine Model of Pancreatic Cancer by Modulation of VEGF Levels and Arginase Activity
- in-vivo, PC, Panc02
TumW↓, We found that diclofenac treatment (30 mg/kg/bw for 11 days) of mice inoculated with PANC02 cells, reduced the tumor weight by 60%, correlating with increased apoptosis of tumor cells.
Apoptosis↑,
VEGF↓, diclofenac drastically decreased tumor vascularization by downregulating VEGF in the tumor and in abdominal cavity fluid.
COX2↓, in contrast to other COX-2 inhibitors, diclofenac increased arginase activity/arginase 1 protein content in tumor stroma cells, peritoneal macrophages and white blood cells by 2.4, 4.8 and 2 fold, respectively.
ARG1/2↑, Diclofenac increases arginase activity in pancreatic tumors and in peritoneal macrophages, but not in bone marrow-CD 115 positive and CD 115 negative cells
TumCG↓, Diclofenac inhibits tumor growth in an orthotopic model of pancreatic cancer in mice
angioG↓, Tumors from diclofenac treated animals were very pale (Fig 1A), suggesting that the treatment caused an antiangiogenic effect.
ARG↓, subsequent arginine depletion and decrease in NO levels, both in serum and peritoneal cavity, adds to tumor growth inhibition by malnourishment and poor vasculature development.
NO↓,


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:


NA, unassigned(tgid=0)

ARG↓, 1,  

Cell Death(tgid=5)

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

TumCG↓, 1,  

Migration(tgid=13)

ARG1/2↑, 1,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 1,   NO↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2↓, 1,  

Functional Outcomes(tgid=23)

TumW↓, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ARG, Arginine
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#:1524  State#:%  Dir#:1
wNotes=on sortOrder:rid,rpid

 

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