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.
RCC, Renal cell Carcinoma: Click to Expand ⟱
Renal cell carcinoma (RCC) is one of the most common malignant tumors of the urinary system, accounting for 80–90% of kidney neoplasms.
The activation of the mTOR pathway has been found in RCC and is correlated with high grade and poor prognostic patient features (41,42).
Scientific Papers found: Click to Expand⟱
5740- Buty,    A Review of Nutritional Regulation of Intestinal Butyrate Synthesis: Interactions Between Dietary Polysaccharides and Proteins
- Review, RCC, NA
*eff↓, Dose↝, eff↑, HDAC↓, ac‑H3↓, ac‑H4↓, *HCAR2↑, *Inflam↓, *ROS↓, *NRF2↑, *GSH↑, *CLDN1↑, *ZO-1↑, IL1β↓, IL6↓, COX2↓, eff↝, eff↑, other↝,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Transcription & Epigenetics ⓘ

ac‑H3↓, 1,   ac‑H4↓, 1,   other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   IL6↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↑, 2,   eff↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Kinase & Signal Transduction ⓘ

HCAR2↑, 1,  

Migration ⓘ

CLDN1↑, 1,   ZO-1↑, 1,  

Immune & Inflammatory Signaling ⓘ

HCAR2↑, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  
Total Targets: 9

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

 

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