HMTs Cancer Research Results

HMTs, Histone methyltransferases (HMTs): Click to Expand ⟱
Source:
Type:
Histone methyltransferases (HMTs) are enzymes that catalyze the addition of methyl groups to histones, leading to chromatin modifications that regulate gene expression. Altered expression and activity of various HMTs have been implicated in cancer initiation, progression, and response to therapy. However, given the diversity of HMT family members (e.g., EZH2, SETDB1, SUV39H1/2, DOT1L, MLL family members), the prognostic associations can vary considerably depending on the specific enzyme and cancer type.

– High levels of some HMTs (e.g., EZH2) are often linked to advanced disease stage and poorer survival
• Enzyme-Specific Effects: The prognostic value largely depends on which HMT is altered. For instance, while overexpression of EZH2 is commonly a marker of poor prognosis, some HMTs may act as tumor suppressors, and their loss could be associated with aggressive behavior.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
7185- 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↓, ROS↑, p‑ATM↑, YAP/TEAD↑, p‑JNK↑, TumPF↓, SUV39H↓, TrxR↓, Casp3↑, Trx1↓, H3↓, lactateProd↓, ATP↓, GlucoseCon↓, TumCG↓, Dose↝,
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↓, ROS↑, YAP/TEAD↑, ATM↑, JNK↑, Apoptosis↑, GlucoseCon↓, lactateProd↓, ATP↓, TumCP↓, TrxR↓, Trx1↓, H3K9↓, p‑ATM↑, γH2AX↑, ALDOB↑, ENO3↑, FBP1↑, GSK‐3β↑, HK3↑, PCK1↑, PGK2↑, PGM1↑, PGM3↑, PHKG1↑, PKLR↑, HK2↓, PCNA↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

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,   SUV39H↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,   Trx1↓, 2,   TrxR↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FBP1↑, 1,   GlucoseCon↓, 2,   HK2↓, 1,   lactateProd↓, 2,   PCK1↑, 1,   PGM1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   JNK↑, 1,   p‑JNK↑, 1,   YAP/TEAD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

H3↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑ATM↑, 2,   PCNA↓, 1,   γH2AX↑, 1,  

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

GSK‐3β↑, 1,   HMTs↓, 2,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,   TumPF↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: HMTs, Histone methyltransferases (HMTs)
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:27  Cells:%  prod#:%  Target#:1096  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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