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.
Scientific Papers found: Click to Expand⟱
2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, *Inflam↓, *antiOx↑, *BioAv↓, *AP-1↓, *NF-kB↓, *HATs↓, *HDAC↑, Dose↑, *ROS↓, *cognitive↑, *Aβ↓,
3234- EGCG,  Rad,    EGCG, a tea polyphenol, as a potential mitigator of hematopoietic radiation injury in mice
- in-vivo, Nor, NA
*DNMTs↓, *radioP↑, *HDAC↑,
3193- SFN,    Epigenetic Therapeutics Targeting NRF2/KEAP1 Signaling in Cancer Oxidative Stress
- Review, Var, NA
DNMTs↓, HDAC↑, NRF2↑, DNMT1↓, DNMT3A↓, NQO1↑, COMT↑, TumCG↓, *toxicity↓,

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:


Redox & Oxidative Stress ⓘ

NQO1↑, 1,   NRF2↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↑, 1,   TumCG↓, 1,  

Hormonal & Nuclear Receptors ⓘ

COMT↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↑, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Transcription & Epigenetics ⓘ

HATs↓, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↑, 2,  

Migration ⓘ

AP-1↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   neuroP↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 14

Scientific Paper Hit Count for: HDAC, Histone deacetylases
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Radiotherapy/Radiation
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#:140  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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