HK3 Cancer Research Results

HK3, hexokinase 3: Click to Expand ⟱
Source:
Type:

HK3 (hexokinase 3) is a glucose-phosphorylating enzyme that catalyzes the first committed step of glycolysis, converting glucose to glucose-6-phosphate. HK3 is expressed prominently in hematopoietic and myeloid cells but is also dysregulated in several cancers. Increased HK3 expression has been associated with enhanced glycolytic activity, higher tumour grade, immune-cell infiltration and poorer prognosis in cancers including glioma and some hematologic malignancies. In glioma, high HK3 expression correlates with malignancy and an immunosuppressive tumour microenvironment enriched in macrophages and other infiltrating immune cells. However, HK3 can also support antitumour immune-cell metabolism in certain contexts, so its biological effect is not universally oncogenic. The typical tumour-associated direction is often up, while the desired direct tumour-cell modulation is generally down; immune-cell effects should be interpreted separately.



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: HK3, hexokinase 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#:1597  State#:%  Dir#:2
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