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.
Scientific Papers found: Click to Expand⟱
1435- GEN,  SFN,    The Effects of Combinatorial Genistein and Sulforaphane in Breast Tumor Inhibition: Role in Epigenetic Regulation
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
DNMTs↓, GEN extensively studied for its role as DNA methyltransferase (DNMT) inhibitor
HDAC↓, SFN), is known as a histone deacetylase (HDAC) inhibitor
eff↑, Our results indicate that the combination of GEN and SFN is much more effective than their single doses in increasing the rate of apoptosis
TumCCA↑, G2 phase in MDA-MB-231 and G1 phase in MCF-7
HMTs↓, histone methyltransferase (HMT) inhibitor
HDAC2↓, combination downregulates the levels of HDAC2 and HDAC3 both at the mRNA and protein levels
HDAC3↓,
KLF4↓, potential to downregulate KLF4 levels, which plays an important role in stem cell formation.
hTERT/TERT↓,

3359- QC,    Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells
- in-vitro, Cerv, HeLa
DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
HDAC2↓,
HDAC6↓,
HDAC11↓,
G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
PTEN↑,
SOCS1↑,

3360- QC,    Role of Flavonoids as Epigenetic Modulators in Cancer Prevention and Therapy
- Review, Var, NA
HDAC↓, Quercetin modulates the expression of various chromatin modifiers and declines the activity of HDACs, DNMTs and HMTs in a dose-dependent manner in human cervical cancer (HeLa) cells
DNMTs↓,
HMTs↓,
Let-7↑, Quercetin also induced let-7c which decreased pancreatic tumor growth by posttranscriptional activation of Numbl and indirect inhibition of Notch
NOTCH↓,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

hTERT/TERT↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,  

DNA Damage & Repair ⓘ

DNMT3A↓, 1,   DNMTs↓, 3,   G9a↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 3,   HDAC1↓, 1,   HDAC11↓, 1,   HDAC2↓, 2,   HDAC3↓, 1,   HDAC6↓, 1,   HMTs↓, 3,   KLF4↓, 1,   Let-7↑, 1,   NOTCH↓, 1,   PTEN↑, 1,  

Migration ⓘ

TIMP3↑, 1,  

Immune & Inflammatory Signaling ⓘ

SOCS1↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 1,   hTERT/TERT↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: HMTs, Histone methyltransferases (HMTs)
2 Quercetin
1 Genistein (soy isoflavone)
1 Sulforaphane (mainly Broccoli)
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#:1096  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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