cGAS–STING Cancer Research Results

cGAS–STING, GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING): Click to Expand ⟱
Source:
Type:
cGAS–STING pathway is primarily associated with neuroinflammation and neuronal damage.
-Studies show upregulated STING in microglia and astrocytes in AD models.
Scientific Papers found: Click to Expand⟱
5511- bemA,    Inhibition of ACLY overcomes cancer immunotherapy resistance via polyunsaturated fatty acids peroxidation and cGAS-STING activation
- in-vitro, Var, NA
ACLY↓, Here, we show that ACLY inhibition up-regulates PD-L1 immune checkpoint expression in cancer cells
PD-L1↑,
mtDam↑, Mechanistically, ACLY inhibition causes polyunsaturated fatty acid (PUFA) peroxidation and mitochondrial damage, which triggers mitochondrial DNA leakage to activate the cGAS-STING innate immune pathway.
cGAS–STING↑, ACLY inhibition leads to cGAS-STING activation
LDL↓, bempedoic acid (BemA; also named ETC-1002) has been recently approved by U.S. Food and Drug Administration (FDA) for lowering low-density lipoprotein cholesterol
eff↑, dietary PUFA supplementation is sufficient to mimic the enhanced efficacy of PD-L1 blockade by ACLY inhibition, providing promising combinational strategies for immunotherapy-resistant tumors therapy.

5988- Chit,    Chitosan immunomodulation: insights into mechanisms of action on immune cells and signaling pathways
- Review, Var, NA
DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)


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 ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   LDL↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT1↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Imm↑, 1,   PD-L1↑, 1,  

Cellular Microenvironment ⓘ

cGAS–STING↑, 2,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

DDS↑, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

PD-L1↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Migration ⓘ

Cartilage↑, 1,   TGF-β1↓, 1,  

Immune & Inflammatory Signaling ⓘ

DCells↑, 1,   IL10↓, 1,   TNF-α↓, 1,  

Functional Outcomes ⓘ

Wound Healing↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: cGAS–STING, GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING)
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#:1370  State#:%  Dir#:2
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