H3K9 Cancer Research Results

H3K9, histone H3 lysine 9: Click to Expand ⟱
Source:
Type:

H3K9 (histone H3 lysine 9) is a major regulatory residue on histone H3 that can undergo methylation or acetylation to alter chromatin structure and gene expression. Methylated H3K9, particularly H3K9me2 and H3K9me3, is generally associated with transcriptional repression and heterochromatin formation, whereas H3K9ac is associated with more transcriptionally active chromatin. In cancer, abnormal regulation of H3K9 modifications can contribute to silencing of tumour-suppressor genes, altered differentiation, stemness and treatment resistance. H3K9 should therefore be treated as an umbrella epigenetic target, with specific marks such as H3K9me3



Scientific Papers found: Click to Expand⟱
7179- CHA,    Chaetocin disrupts the SUV39H1–HP1 interaction independent of SUV39H1 methyltransferase activity
- in-vitro, NA, NA
H3K9↓, SUV39H↓,
7183- CHA,    The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells
- in-vitro, AML, HL-60 - in-vitro, AML, KG-1 - in-vitro, lymphoma, U937
TumCD↓, SUV39H↓, CD11b↑, Diff↑, H3K9↓, eff↑,
7186- CHA,  TSA,    Improved Therapeutic Effect against Leukemia by a Combination of the Histone Methyltransferase Inhibitor Chaetocin and the Histone Deacetylase Inhibitor Trichostatin A
- in-vitro, AML, NA
SUV39H↓, H3K9↓, eff↑,
7171- CHA,    Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201
- vitro+vivo, GBM, DIPG
TumCG↓, TumCP↓, Apoptosis↓, OS↑, H3K9↓, SUV39H↓, eff↑, CSCs↓, SOX9↓, HGF/c-Met↓, FGF21↓, EGFR↓, PDGFR-BB↓, Wnt↓, MYCN↑, OLIG2↓, AURKB↓, HO-1↑, P21↑,
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↓,
7162- CHA,    Chaetocin disrupts the SUV39H1-HP1 interaction independent of SUV39H1 methyltransferase activity
- Study, Nor, NA
*H3K9↓, *other↓, *SUV39H↓,
7161- CHA,    Chaetocin is a nonspecific inhibitor of histone lysine methyltransferases
- Review, Var, NA
H3K9↓, HKMT↓, SUV39H↓, Dose↝,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0)

ALDOB↑, 1,   AURKB↓, 1,   ENO3↑, 1,   H3K9↓, 6,   HK3↑, 1,   HKMT↓, 1,   MYCN↑, 1,   OLIG2↓, 1,   PGK2↑, 1,   PGM3↑, 1,   PHKG1↑, 1,   PKLR↑, 1,   SUV39H↓, 5,  

Redox & Oxidative Stress(tgid=1)

HO-1↑, 1,   ROS↑, 1,   Trx1↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3)

ATP↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

FBP1↑, 1,   FGF21↓, 1,   GlucoseCon↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PCK1↑, 1,   PGM1↑, 1,  

Cell Death(tgid=5)

Apoptosis↓, 1,   Apoptosis↑, 1,   HGF/c-Met↓, 1,   JNK↑, 1,   TumCD↓, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6)

SOX9↓, 1,  

DNA Damage & Repair(tgid=10)

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

Cell Cycle & Senescence(tgid=11)

P21↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

CSCs↓, 1,   Diff↑, 1,   GSK‐3β↑, 1,   HMTs↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13)

CD11b↑, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14)

EGFR↓, 1,   PDGFR-BB↓, 1,  

Drug Metabolism & Resistance(tgid=21)

Dose↝, 1,   eff↑, 3,  

Clinical Biomarkers(tgid=22)

EGFR↓, 1,  

Functional Outcomes(tgid=23)

OS↑, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

H3K9↓, 1,   SUV39H↓, 1,  

Transcription & Epigenetics(tgid=7)

other↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: H3K9, histone H3 lysine 9
7 chaetocin
1 Trichostatin A
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#:1593  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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