ASC Cancer Research Results

ASC, Apoptosis-associated Speck-like protein containing a CARD: Click to Expand ⟱
Source:
Type:
ASC (Apoptosis-associated Speck-like protein containing a CARD, also known as PYCARD) – ASC is a key adaptor molecule in the assembly of inflammasomes—a multiprotein complex that activates caspase-1.
– Beyond its inflammasome functions, ASC has been implicated in mediating apoptosis.

– In some cancers, ASC expression is downregulated, which may impair inflammasome assembly and promote immune evasion, whereas in other tumor types, elevated ASC has been reported, sometimes reflecting a heightened local inflammatory state.
– Studies indicate that reduced ASC expression in certain tumor types (for example, melanoma or colon cancer) can correlate with decreased inflammasome activity, potentially leading to immune evasion and a more aggressive tumor phenotype.
– Conversely, in some cancers an upregulation or persistent activation of ASC-containing inflammasomes has been linked to a pro-inflammatory milieu that might drive tumor progression and metastasis.
Scientific Papers found: Click to Expand⟱
3420- TQ,    Thymoquinone alleviates the accumulation of ROS and pyroptosis and promotes perforator skin flap survival through SIRT1/NF-κB pathway
- in-vitro, Nor, HUVECs - in-vitro, NA, NA
*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   ROS↓, 1,   SOD1↑, 1,  

Core Metabolism/Glycolysis ⓘ

SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp1↓, 1,   Pyro?, 1,  

Migration ⓘ

MMP9↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   eNOS↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC?, 1,   IL18↓, 1,   IL1β↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 17

Scientific Paper Hit Count for: ASC, Apoptosis-associated Speck-like protein containing a CARD
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

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