PGM3 Cancer Research Results

PGM3, phosphoglucomutase 3: Click to Expand ⟱
Source:
Type:

PGM3 (phosphoglucomutase 3; phosphoacetylglucosamine mutase) is an enzyme of the hexosamine biosynthetic pathway that catalyzes the interconversion of N-acetylglucosamine-6-phosphate and N-acetylglucosamine-1-phosphate, thereby supporting production of UDP-N-acetylglucosamine (UDP-GlcNAc). UDP-GlcNAc is required for protein N-glycosylation, O-GlcNAcylation and other glycosylation reactions that regulate cell signalling, metabolism and protein stability. PGM3 is upregulated in several cancers and can promote tumour-cell proliferation, migration, metabolic reprogramming and survival. In colorectal cancer, increased PGM3 supports O-GlcNAcylation and maintains β-catenin signalling, whereas PGM3 knockdown reduces proliferation and migration. In bladder cancer, elevated PGM3 promotes both glycolysis and oxidative phosphorylation and is associated with tumour growth, metastasis and poorer prognosis. The typical cancer-associated direction is therefore generally up, while the desired anticancer modulation is down or enzyme inhibition.



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: PGM3, phosphoglucomutase 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#:1599  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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