HDAC Cancer Research Results

HDAC, Histone deacetylases: Click to Expand ⟱
Source:
Type:
Enzymes involved in regulating gene expression by removing acetyl groups from histones, the proteins around which DNA is wrapped.
-Many cancers exhibit altered expression levels of HDACs, which can contribute to the dysregulation of genes involved in cell growth, survival, and differentiation.
-HDACs can repress the expression of tumor suppressor genes, leading to uncontrolled cell proliferation and survival. This repression can be a key factor in the development and progression of cancer.
-HDAC inhibitors (HDACi) have been developed and are being investigated for their ability to reactivate silenced genes, induce cell cycle arrest, and promote apoptosis in cancer cells.
-HDAC1, HDAC2): Often overexpressed in various cancers, including breast, prostate, and colorectal cancers. Their overexpression is associated with poor prognosis.
-HDAC4, HDAC5): These may have both oncogenic and tumor-suppressive roles depending on the context and cancer type.
-While HDACs are not classified as traditional oncogenes, their overexpression and activity can contribute to oncogenic processes.
-HDAC inhibitor works by preventing the removal of acetyl groups from histones, thereby modulating gene expression, influencing cell behavior, and potentially reversing aberrant gene silencing seen in various diseases.
-HDAC inhibitors can help reactivate these genes, thereby inhibiting growth and inducing apoptosis in cancer cells.
AML, Acute Myeloid Leukemia: Click to Expand ⟱
Acute Myeloid Leukemia
Scientific Papers found: Click to Expand⟱
3357- QC,    The polyphenol quercetin induces cell death in leukemia by targeting epigenetic regulators of pro-apoptotic genes
- in-vitro, AML, HL-60 - NA, NA, U937
DNMT1↓, DNMT3A↓, HDAC↓, ac‑H3↑, ac‑H4↑, BAX↑, APAF1↑, BNIP3↑, STAT3↑,
3426- TQ,    Thymoquinone-Induced Reactivation of Tumor Suppressor Genes in Cancer Cells Involves Epigenetic Mechanisms
- in-vitro, BC, MDA-MB-468 - in-vitro, AML, JK
UHRF1↓, DNMT1↓, DNMT3A↓, DNMTs↓, HDAC1↓, HDAC4↓, HDAC↓, DLC1↑, PPARγ↑, FOXO↑, TET2↑, CYP1B1↑, G9a↓,

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:


Core Metabolism/Glycolysis ⓘ

PPARγ↑, 1,  

Cell Death ⓘ

APAF1↑, 1,   BAX↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

CYP1B1↑, 1,   DNMT1↓, 2,   DNMT3A↓, 2,   DNMTs↓, 1,   G9a↓, 1,   UHRF1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,   HDAC↓, 2,   HDAC1↓, 1,   HDAC4↓, 1,   STAT3↑, 1,  

Migration ⓘ

DLC1↑, 1,  

Drug Metabolism & Resistance ⓘ

TET2↑, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: HDAC, Histone deacetylases
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:2  Cells:%  prod#:%  Target#:140  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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