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.
GC, Gastric Adenocarcinoma: Click to Expand ⟱
Stomach/Gastric Cancer
Scientific Papers found: Click to Expand⟱
2631- Api,    Apigenin Induces Autophagy and Cell Death by Targeting EZH2 under Hypoxia Conditions in Gastric Cancer Cells
- in-vivo, GC, NA - in-vitro, GC, AGS
ER Stress↑, Hif1a↓, EZH2↓, HDAC↓, TumAuto↑, p‑mTOR↓, AMPKα↑, GRP78/BiP↑, ROS↑, MMP↓, Ca+2↑, ATF4↑, CHOP↑,
1452- SFN,    Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
- in-vitro, GC, AGS
MMP9↓, p38↓, ERK↓, AP-1↓, ROS↓, NF-kB↓, TumCI↓, MMP9↓, HDAC↓, Glycolysis↓, Hif1a↓, *memory↑, *cognitive↑,

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:


Redox & Oxidative Stress ⓘ

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,  

Cell Death ⓘ

p38↓, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   HDAC↓, 2,   p‑mTOR↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 1,   MMP9↓, 2,   TumCI↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   Hif1a↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 1,  
Total Targets: 2

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:28  Cells:%  prod#:%  Target#:140  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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