ARG1/2 Cancer Research Results

ARG1/2, Arginases ARG1/2: Click to Expand ⟱
Source:
Type:
Arginases are key enzymes that hydrolyze L-arginine to urea and L-ornithine in the urea cycle.
The two arginase isoforms, arginase 1 (ARG1) and arginase 2 (ARG2), regulate the proliferation of cancer cells, migration, and apoptosis; affect immunosuppression; and promote the synthesis of polyamines, leading to the development of cancer. Arginases also compete with nitric oxide synthase (NOS) for L-arginine, and their participation has also been confirmed in cardiovascular diseases, stroke, and inflammation.
ARG1 is a much more explored isoform of arginase localized in the cytosol and is expressed mainly in the liver.
ARG2, also called mitochondrial arginase, is expressed in extrahepatic tissues, i.e., the kidneys, small intestine, prostate, and mammary gland.
Arginases are biomarkers and can be used to track disease progression [33]. Targeting ARG1 and ARG2 has been proposed for various diseases. Currently, a dual inhibitor of arginases is under validation in clinical trials in patients with solid tumors; OATD-02 targets both extracellular and intracellular ARG1 and ARG2.
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↓,

204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG1/2↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

2213- SK,    Shikonin attenuates cerebral ischemia/reperfusion injury via inhibiting NOD2/RIP2/NF-κB-mediated microglia polarization and neuroinflammation
- in-vivo, Stroke, NA
*neuroP↑, Shikonin treatment significantly reduced brain infarction volume and improved neurological function in MCAO/R rats.
*Inflam↓, Shikonin treatment significantly reduced microglial proinflammatory phenotype and levels of proinflammatory markers (inducible-NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α),
*iNOS↓,
*TNF-α↓,
*IL1β↓, interleukin-1 beta (IL-1β), and IL-6), increased microglial anti-inflammatory phenotype and levels of anti-inflammatory markers (Arginase-1 (Arg1), transforming growth factor-beta (TGF-β), and IL-10),
*IL6↓,
*ARG1/2↑,
*TGF-β↑,
*IL10↑,
*NF-kB↓, reversed the expression of Nucleotide-binding oligomerization domain 2 (NOD2) and phosphorylation receptor interacting protein 2 (p-RIP2), and suppressed nuclear factor kappa-B (NF-κB) signaling activation in the ischemic penumbra regions.
*eff↓, Furthermore, overexpression of NOD2 markedly attenuated the neuroprotective effects of Shikonin treatment in MCAO/R rats.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

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:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 2,   p‑JNK↓, 1,   MAPK↓, 1,   p‑p38↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,  

Migration(tgid=13) ⓘ

ARG1/2↑, 2,   TGF-β↑, 1,   TGF-β1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

p‑IKKα↓, 1,   IL1↓, 1,   IL10↑, 2,   IL1β↓, 1,   IL4↑, 1,   IL6↓, 2,   Inflam↓, 1,   p‑IκB↓, 1,   MyD88↓, 1,   NF-kB↓, 2,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 29

Scientific Paper Hit Count for: ARG1/2, Arginases ARG1/2
1 Diclofenac
1 Magnetic Field Rotating
1 Magnetic Fields
1 Shikonin
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#:560  State#:%  Dir#:2
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