PHKG1 Cancer Research Results

PHKG1, phosphorylase kinase catalytic subunit gamma 1: Click to Expand ⟱
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PHKG1 (phosphorylase kinase catalytic subunit gamma 1) is the catalytic gamma subunit of phosphorylase kinase, a serine/threonine kinase complex that activates glycogen phosphorylase and thereby promotes glycogenolysis. PHKG1 therefore links hormonal and calcium-dependent signalling with mobilization of stored glycogen and production of glucose-1-phosphate for energy metabolism. Because many tumour cells can use glycogen as a metabolic reserve during hypoxia, nutrient limitation and other stress, increased phosphorylase-kinase activity may support tumour metabolic adaptation. However, PHKG1 itself is not yet established as a broadly oncogenic driver or therapeutic target across cancers. Its cancer-associated direction should therefore be considered context-dependent or insufficiently established unless a study directly demonstrates PHKG1 upregulation, activation or dependency. PHKG1 is separate from PHKG2 and from downstream glycogen phosphorylases such as PYGL, PYGB and PYGM.



Scientific Papers found: Click to Expand⟱
7167- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
YAP/TEAD↑, Increased intracellular ROS induced (i) Yes-associated protein 1 (YAP1) expression independent of the canonical Hippo pathway as well as (ii) ATM and JNK activation.
ATM↑,
JNK↑,
Apoptosis↑, Increased interaction of YAP1 with p73 and p300 induced apoptosis in an ATM-dependent manner.
GlucoseCon↓, decreased ATP production was accompanied by a ROS/JNK-dependent decrease in cellular glucose uptake by glioma cells in the presence of Chaetocin
lactateProd↓, A significant decrease in lactate production (Figure 5d) and ATP generation (Figure 5e) was observed in Chaetocin-treated cells as compared with the untreated control.
ATP↓,
TumCP↓, Chaetocin inhibits glioma cell proliferation
TrxR↓, Chaetocin treatment reduced thioredoxin reductase activity in a dose-dependent manner with ∼40% decrease in activity observed at 1 μM concentration
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3K9↓, The decrease in H3K9me3 levels observed upon Chaetocin treatment was reverted in the presence of ROS inhibitor NAc
p‑ATM↑, Chaetocin induced an increase in pATM and γH2AX expression in a ROS-dependent manner
γH2AX↑,
ALDOB↑, ALDOB, ENO3, FBP1, FBP2 G6PC, GCK GSK3B, GYS2, HK3, PCK1, PGK2, PGM3, PHKG1, PKLR, PRPS1L1 and PYGM) were elevated by more than 2 fold upon Chaetocin treatment
ENO3↑,
FBP1↑,
GSK‐3β↑,
HK3↑,
PCK1↑,
PGK2↑,
PGM1↑,
PGM3↑,
PHKG1↑,
PKLR↑, PKLR, up-regulated by 20.9
HK2↓, HK2, downregulated by 4.5 fold
PCNA↓, Decrease in both PCNA-positive cells and its protein level in Chaetocin-treated tumors indicated inhibition of cell proliferation


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) ⓘ

ALDOB↑, 1,   ENO3↑, 1,   H3K9↓, 1,   HK3↑, 1,   PGK2↑, 1,   PGM3↑, 1,   PHKG1↑, 1,   PKLR↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,   Trx1↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FBP1↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PCK1↑, 1,   PGM1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   JNK↑, 1,   YAP/TEAD↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑ATM↑, 1,   PCNA↓, 1,   γH2AX↑, 1,  

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

GSK‐3β↑, 1,   HMTs↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  
Total Targets: 28

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PHKG1, phosphorylase kinase catalytic subunit gamma 1
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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