ATG3 Cancer Research Results

ATG3, Autophagy-related 3: Click to Expand ⟱
Source:
Type: protein
ATG3 (Autophagy-related 3) is a protein that plays a crucial role in the process of autophagy, a cellular mechanism that involves the degradation and recycling of damaged or dysfunctional cellular components. ATG3 is involved in the regulation of autophagy.
Increased expression in: breast, lung, GBM, ovarian, prostate, panreatic, hepatocellar.
Decreased expression in: colon (associated with improved prognosis).
Scientific Papers found: Click to Expand⟱
1871- DAP,    Targeting PDK1 with dichloroacetophenone to inhibit acute myeloid leukemia (AML) cell growth
- in-vitro, AML, U937 - in-vivo, AML, NA
TumCP↓, DAP significantly inhibited cell proliferation, increased apoptosis induction and suppressed autophagy in AML cells in vitro
Apoptosis↑,
TumCG↓, inhibited tumor growth in an AML mouse model in vivo
PDK1↓, inhibition of PDK1 with DAP
cl‑PARP↑, increased the cleavage of pro-apoptotic proteins (PARP and Caspase 3)
Bcl-xL↓, decreased the expression of the anti-apoptotic proteins (BCL-xL and BCL-2) and autophagy regulators (ULK1, Beclin-1 and Atg).
Bcl-2↓,
Beclin-1↓,
ATG3↓,
PI3K↓, DAP inhibited the PI3K/Akt signaling pathway
Akt↓,
eff↑, Importantly, 2,2-dichloroacetophenone (DAP) is a much more potent inhibitor of PDK1(than DCA). It is effective at concentrations in the micromolar (μM) range.

4735- SeNPs,    Selenium triggers Nrf2-AMPK crosstalk to alleviate cadmium-induced autophagy in rabbit cerebrum
- in-vivo, Nor, NA
*MDA↓, Se decreased the contents of MDA and H2O2 and increased the activities of CAT, SOD, GST, GSH and GSH-Px, alleviating the imbalance of the redox system induced by Cd.
*H2O2↓,
*Catalase↑,
*SOD↑,
*GSTs↑,
*GSH↑,
*NRF2↓, Cd caused the up-regulation of the mRNA levels of autophagy-related genes (ATG3, ATG5, ATG7, ATG12 and p62), AMPK (Prkaa1, Prkaa2, Prkab1, Prkab2, Prkag2, Prkag3) and Nrf2 (Nrf2, HO-1 and NQO
*ATG3↓, which were alleviated by Se, indicated that Se inhibited Cd-induced autophagy and Nrf2 signaling pathway activation
*AMPK↓,
*ROS↓, our study found that Se antagonized Cd-induced oxidative stress and autophagy in the brain by generating crosstalk between AMPK and Nrf2 signaling pathway.


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:


Core Metabolism/Glycolysis ⓘ

PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↓, 1,   Beclin-1↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GSH↑, 1,   GSTs↑, 1,   H2O2↓, 1,   MDA↓, 1,   NRF2↓, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↓, 1,  
Total Targets: 10

Scientific Paper Hit Count for: ATG3, Autophagy-related 3
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#:722  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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