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.


GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.

Scientific Papers found: Click to Expand⟱
2663- AL,    Therapeutic Effect of Allicin on Glioblastoma
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG
BioAv↝, TumCCA↑, P53↑, HDAC↓, CSCs↓, ROS↑, ChemoSen↑, MGMT↓,
2026- PB,    Oral sodium phenylbutyrate in patients with recurrent malignant gliomas: A dose escalation and pharmacologic study
- Trial, GBM, NA
Dose↝, Dose↑, Dose↝, OS↑, HDAC↓, TumCCA↑, P21↑, other↝, BioAv↑, eff↑,
2045- PB,    Phenylbutyrate—a pan-HDAC inhibitor—suppresses proliferation of glioblastoma LN-229 cell line
- in-vitro, GBM, LN229 - in-vitro, GBM, LN-18
HDAC↓, TumCG↓, TumCCA↑, P21↑, Bcl-2↓, Bcl-xL↓, BioAv↑,
1062- SSE,    Sodium Selenite Decreased HDAC Activity, Cell Proliferation and Induced Apoptosis in Three Human Glioblastoma Cells
- in-vitro, GBM, LN229 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HDAC↓, TumCP↓, TumCCA↑, Apoptosis↑, Casp3↝, MMP2↓, *BioAv↝,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↑, 1,  

Cell Death

Apoptosis↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↝, 1,  

Transcription & Epigenetics

other↝, 1,  

DNA Damage & Repair

MGMT↓, 1,   P53↑, 1,  

Cell Cycle & Senescence

P21↑, 2,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State

CSCs↓, 1,   HDAC↓, 4,   TumCG↓, 1,  

Migration

MMP2↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance

BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 2,   eff↑, 1,  

Functional Outcomes

OS↑, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Drug Metabolism & Resistance

BioAv↝, 1,  
Total Targets: 1

Scientific Paper Hit Count for: HDAC, Histone deacetylases
2 Phenylbutyrate
1 Allicin (mainly Garlic)
1 Selenite (Sodium)
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:27  Cells:%  prod#:%  Target#:140  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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