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.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
1580- Citrate,    Citrate activates autophagic death of prostate cancer cells via downregulation CaMKII/AKT/mTOR pathway
- in-vitro, Pca, PC3 - in-vivo, PC, NA - in-vitro, Pca, LNCaP - in-vitro, Pca, WPMY-1
Apoptosis↑, Ca+2↓, Akt↓, mTOR↓, selectivity↑, TumCP↓, cl‑Casp3↑, cl‑PARP↑, LC3‑Ⅱ/LC3‑Ⅰ↑, p62↓, ATG5↑, ATG7↑, Beclin-1↑, TumAuto↑, CaMKII ↓,

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:


Core Metabolism/Glycolysis ⓘ

ATG7↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   cl‑Casp3↑, 1,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

Ca+2↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

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:22  Cells:%  prod#:%  Target#:986  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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