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.
Liver, Liver Cancer: Click to Expand ⟱
Liver Cancer
Scientific Papers found: Click to Expand⟱
5326- ALC,    L-Carnitine Is an Endogenous HDAC Inhibitor Selectively Inhibiting Cancer Cell Growth In Vivo and In Vitro
- vitro+vivo, Liver, HepG2
TumCG↓, P21↑, ac‑H3↑, HDAC↓, *ATP↑, selectivity↑, ac‑H4↑,
1064- LT,  Cisplatin,    Inhibition of cell survival, invasion, tumor growth and histone deacetylase activity by the dietary flavonoid luteolin in human epithelioid cancer cells
- vitro+vivo, Lung, LNM35 - in-vitro, CRC, HT-29 - in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Casp3↑, Casp7↑, HDAC↓,
2077- PB,    Butyrate induces ROS-mediated apoptosis by modulating miR-22/SIRT-1 pathway in hepatic cancer cells
- in-vitro, Liver, HUH7
miR-22↑, SIRT1↓, ROS↑, Cyt‑c↑, Casp3↑, eff↓, TumCG↓, TumCP↓, HDAC↓, SIRT1↓, CD44↓, proMMP2↓, MMP↓, SOD↓,

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 ⓘ

ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

SIRT1↓, 2,  

Cell Death ⓘ

Casp3↑, 2,   Casp7↑, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   HDAC↓, 3,   TumCG↓, 2,  

Migration ⓘ

miR-22↑, 1,   proMMP2↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   selectivity↑, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: HDAC, Histone deacetylases
1 Acetyl-l-carnitine
1 Luteolin
1 Cisplatin
1 Phenylbutyrate
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:14  Cells:%  prod#:%  Target#:140  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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