ATG7 Cancer Research Results

ATG7, ATG7: Click to Expand ⟱
Source:
Type:
Autophagy Regulator:
– ATG7 is an E1-like enzyme crucial for the autophagy pathway.
– It participates in the conjugation systems that drive autophagosome formation (e.g., ATG12–ATG5 and LC3 lipidation systems).

• Elevated Expression:
– In certain cancers (e.g., pancreatic cancer, some subtypes of breast cancer), ATG7 can be upregulated.
– Increased ATG7 expression in some contexts is thought to help tumors survive under metabolic stress by enhancing autophagy.

• Reduced Expression or Loss-of-Function:
– In other contexts – for instance, in some liver cancers or specific lung cancers – reduced expression or inactivation of ATG7 has been reported.
– This reduction might lead to failure of effective autophagy in tumor-suppressive contexts.
Scientific Papers found: Click to Expand⟱
7837- ISQ,    Isoquercitrin Delays Denervated Soleus Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation
- in-vivo, Nor, NA
*Dose↝, Isoquercitrin demonstrated the optimal protective effect at 20 mg/kg/d, which was the dose used in subsequent experiments.
*autophagy↓, Following isoquercitrin treatment, mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy-related proteins (ATG7, BNIP3, LC3B, and PINK1);
*ATG7↓,
*BNIP3↓,
*LC3B↓,
*PINK1↓,
*ROS↓, (ROS) in the target muscle was reduced, which might be associated with the upregulation of antioxidant factors (SOD1, SOD2, NRF2, NQO1, and HO1) and the downregulation of ROS production-related factors (Nox2, Nox4, and DUOX1).
*SOD1↑,
*SOD2↑,
*NRF2↑,
*NQO1↑,
*HO-1↑,
*NOX2↓,
*NOX4↓,
*DUOX1↓,
*IL1β↓, isoquercitrin treatment reduced the levels of inflammatory factors—interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)—in the target muscle and inactivated the JAK/STAT3 signaling pathway.
*IL6↓,
*TNF-α↓,
*JAK↓,
*STAT3↓,
*Inflam↓, via inhibition of oxidative stress and inflammatory response.


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:


NA, unassigned(tgid=0) ⓘ

autophagy↓, 1,   DUOX1↓, 1,   NOX2↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↑, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PINK1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATG7↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

BNIP3↓, 1,   LC3B↓, 1,  

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

STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   JAK↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  
Total Targets: 22

Scientific Paper Hit Count for: ATG7, ATG7
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#:986  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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