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.
BC, Breast Cancer: Click to Expand ⟱
Breast Cancer
Scientific Papers found: Click to Expand⟱
177- Api,    Inhibition of MDA-MB-231 breast cancer cell proliferation and tumor growth by apigenin through induction of G2/M arrest and histone H3 acetylation-mediated p21WAF1/CIP1 expression
- in-vitro, BC, MDA-MB-231
Cyc↓, CycB/CCNB1↓, CDK1↓, P21↑, PCNA↝, HDAC↓, TumCP↓, TumCCA↑, ac‑H3↑, TumW↓, TumVol↓,
3175- Ash,  SFN,    Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
DNMTs↓, HDAC↓, eff↑,
1433- Ash,  SFN,    A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
eff↑, Bcl-2↓, BAX↑, tumCV↓, DNMT1↓, DNMT3A↓, HDAC↓,
2698- BBR,    A gene expression signature-based approach reveals the mechanisms of action of the Chinese herbal medicine berberine
- Analysis, BC, MDA-MB-231
HDAC↓, Akt↓, mTOR↓, ER Stress↑, TumAuto↑, AMPK↑, mTOR∅, HDAC∅, ac‑α-tubulin↑,
2050- Buty,    The Role of Sodium Phenylbutyrate in Modifying the Methylome of Breast Cancer Cells
- in-vitro, BC, MCF-7
eff↑, HDAC↓, TumCG↓,
2798- CHr,    Chrysin: a histone deacetylase 8 inhibitor with anticancer activity and a suitable candidate for the standardization of Chinese propolis
- in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
HDAC↓, HDAC8↓, TumCG↓, Diff↑,
1435- GEN,  SFN,    The Effects of Combinatorial Genistein and Sulforaphane in Breast Tumor Inhibition: Role in Epigenetic Regulation
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
DNMTs↓, HDAC↓, eff↑, TumCCA↑, HMTs↓, HDAC2↓, HDAC3↓, KLF4↓, hTERT/TERT↓,
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↓,
2046- PB,    Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-468 - in-vitro, Nor, MCF10
Apoptosis↑, i-ROS?, Casp↑, MMP?, selectivity↑, *ROS∅, HDAC↓, DNArepair↓, Casp3↑, Casp8↑, *toxicity↓, TumCCA↑,
2040- SAHA,    The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin
- in-vitro, Pca, LNCaP - in-vitro, CRC, T24/HTB-9 - in-vitro, BC, MCF-7
HDAC↓, TumCG↓, Diff↑, Apoptosis↑, TXNIP↑,
1430- SFN,    Sulforaphane bioavailability and chemopreventive activity in women scheduled for breast biopsy
- Trial, BC, NA
*HDAC3↓, HDAC↓, *toxicity↓,
1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
CardioT↓, *GSH↑, *ROS↓, *NRF2↑, NRF2∅, HDAC↓, DNMTs↓, Casp3↑, ER-α36↓, Remission↑, eff↑, ROS↑, selectivity?,
3426- TQ,    Thymoquinone-Induced Reactivation of Tumor Suppressor Genes in Cancer Cells Involves Epigenetic Mechanisms
- in-vitro, BC, MDA-MB-468 - in-vitro, AML, JK
UHRF1↓, DNMT1↓, DNMT3A↓, DNMTs↓, HDAC1↓, HDAC4↓, HDAC↓, DLC1↑, PPARγ↑, FOXO↑, TET2↑, CYP1B1↑, G9a↓,
3421- TQ,    Insights into the molecular interactions of thymoquinone with histone deacetylase: evaluation of the therapeutic intervention potential against breast cancer
- Analysis, Nor, NA - in-vivo, Nor, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, HaCaT
HDAC↓, P21↑, Maspin↑, BAX↑, B2M↓, TumCCA↑, selectivity↑, *toxicity↓, TumCMig↓, TumCP↓,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2∅, 1,   ROS↑, 1,   i-ROS?, 1,  

Mitochondria & Bioenergetics ⓘ

MMP?, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 3,   Casp7↑, 1,   Casp8↑, 1,   hTERT/TERT↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CYP1B1↑, 1,   DNArepair↓, 1,   DNMT1↓, 2,   DNMT3A↓, 2,   DNMTs↓, 4,   G9a↓, 1,   PCNA↝, 1,   UHRF1↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   Cyc↓, 1,   CycB/CCNB1↓, 1,   P21↑, 2,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 2,   FOXO↑, 1,   HDAC↓, 14,   HDAC∅, 1,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC4↓, 1,   HDAC8↓, 1,   HMTs↓, 1,   KLF4↓, 1,   mTOR↓, 1,   mTOR∅, 1,   TumCG↓, 3,  

Migration ⓘ

DLC1↑, 1,   ER-α36↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TXNIP↑, 1,   ac‑α-tubulin↑, 1,  

Immune & Inflammatory Signaling ⓘ

B2M↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 5,   selectivity?, 1,   selectivity↑, 2,   TET2↑, 1,  

Clinical Biomarkers ⓘ

B2M↓, 1,   hTERT/TERT↓, 1,   Maspin↑, 1,  

Functional Outcomes ⓘ

CardioT↓, 1,   Remission↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   NRF2↑, 1,   ROS↓, 1,   ROS∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC3↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 3,  
Total Targets: 6

Scientific Paper Hit Count for: HDAC, Histone deacetylases
5 Sulforaphane (mainly Broccoli)
2 Ashwagandha(Withaferin A)
2 Thymoquinone
1 Apigenin (mainly Parsley)
1 Berberine
1 Butyrate
1 Chrysin
1 Genistein (soy isoflavone)
1 Luteolin
1 Cisplatin
1 Phenylbutyrate
1 Vorinostat
1 doxorubicin
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:4  Cells:%  prod#:%  Target#:140  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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