PYGL Cancer Research Results

PYGL, glycogen phosphorylase, liver form: Click to Expand ⟱
Source:
Type:

PYGL (glycogen phosphorylase, liver form) is an enzyme that catalyzes glycogen breakdown to glucose-1-phosphate. PYGL is commonly upregulated in cancer, particularly under hypoxic conditions, where it mobilizes stored glycogen to support glycolysis, pentose-phosphate-pathway activity, ATP production and redox homeostasis. Increased PYGL can promote tumour-cell proliferation, survival, migration, invasion and metastasis. Its inhibition or downregulation causes glycogen accumulation, metabolic and replication stress, reduced proliferation and, in some cancer models, senescence or apoptosis. The typical cancer-associated direction is up, while the desired anticancer modulation is down. PYGL is separate from the related isoenzymes PYGB and PYGM.



Scientific Papers found: Click to Expand⟱
7039- Cic,    Chicoric acid targets PYGL to normalize glycogenolysis-driven glycolysis to suppress non-small cell lung cancer
- in-vitro, NSCLC, H1975 - in-vitro, NSCLC, H460
PYGL↓, Glycolysis↓, LDHA↓, lactateProd↓, GlucoseCon↓, TumCP↓,

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:


NA, unassigned(tgid=0)

PYGL↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

GlucoseCon↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   LDHA↓, 1,  

Migration(tgid=13)

TumCP↓, 1,  
Total Targets: 6

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PYGL, glycogen phosphorylase, liver form
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#:1568  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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