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.
PSA, Psoriasis: Click to Expand ⟱
Psoriasis is an autoimmune skin disease.
This section mainly deals with PsA which is psoriatic arthritis

PsA evidence based approach

Rank Approach Evidence Mechanism / Rationale Notes
1 Weight loss if overweight/obese Best direct evidence in PsA Reduces metabolic inflammation, adipokine burden, and joint inflammatory load; may improve treatment response. Highest-yield natural strategy when excess weight is present.
2 Regular exercise / physical activity Good supportive evidence Improves pain, stiffness, function, fatigue, muscle support, and cardiometabolic health. Strong adjunct for joint symptoms and overall health.
3 Mediterranean-style diet / antioxidant-rich whole-food diet Moderate evidence May reduce systemic inflammatory tone; provides polyphenols, fiber, unsaturated fats, and better metabolic support. Best antioxidant strategy is diet pattern rather than antioxidant pills.
4 Intermittent fasting / time-restricted eating Early limited evidence May improve inflammatory signaling and metabolic regulation; possible benefit for CRP, enthesitis, and disease activity. Promising but still exploratory.
5 Omega-3 (fish / fish oil) Mixed evidence Shifts eicosanoids toward less inflammatory profiles and may modestly reduce inflammatory tone. Reasonable adjunct, but not a top-tier PsA joint intervention.
6 Vitamin D Weak PsA-specific treatment evidence More relevant for deficiency correction, bone support, and immune modulation than for direct joint control. Most relevant when levels are low.

PsA pathways to modulate

Rank Pathway / Axis Why It Matters in PsA Joints Helpful Modulation Support Level
1 IL-23 → Th17/Tc17 → IL-17A/F Core inflammatory axis in psoriatic arthritis; active in synovium, enthesis, and related tissues. Reduce excessive IL-23 / IL-17 signaling and downstream cytokine/chemokine output. Very high
2 TNF-α / NF-κB inflammatory axis Major validated cytokine pathway driving inflammation, tissue injury, and amplification of disease activity. Reduce TNF / NF-κB-driven inflammatory signaling and matrix damage. Very high
3 JAK / STAT3 signaling Supports cytokine signaling relevant to synovial and entheseal inflammation. Dampen excessive JAK / STAT3 inflammatory activity. High
4 Myeloid / inflammasome amplification (IL-1β, IL-6, GM-CSF) Amplifies synovitis, pain, recruitment of inflammatory cells, and osteoclastogenic signaling. Reduce IL-1β, IL-6, and GM-CSF inflammatory amplification. High
5 RANKL / M-CSF / osteoclastogenesis Important for bone erosions and osteoclast-mediated damage. Reduce osteoclast differentiation and bone resorption pressure. High
6 DKK1 / Wnt / BMP bone-remodeling balance PsA involves both erosions and abnormal new bone formation. Rebalance remodeling rather than simply suppress all bone formation. Moderate to high
7 COX-2 / 5-LOX / eicosanoid signaling Contributes to inflammatory pain, swelling, and leukocyte recruitment. Reduce excess prostaglandin and leukotriene inflammatory tone. Moderate
8 KEAP1-NRF2 / oxidative stress-redox balance Oxidative imbalance may reinforce inflammatory signaling and tissue injury. Improve antioxidant defense and redox resilience. Moderate
9 Obesity / adipokine / metabolic inflammation axis Obesity is linked to worse disease activity and poorer response. Reduce metabolic inflammation and adverse adipokine signaling. Moderate
10 Gut microbiome / barrier / immune-metabolite axis Gut dysbiosis and barrier changes may influence systemic immune activation. Support gut barrier function and more favorable immune-metabolic signaling. Moderate

Natural products that might help PsA — mechanistic HTML table

Natural Product / Class Main PsA-Relevant Pathways Mechanistic Rationale Direct PsA Joint Evidence Practical Read
Omega-3 (EPA/DHA) IL-17-related signaling; TNF/NF-κB tone; eicosanoids / resolution pathways May shift lipid mediators toward less inflammatory profiles and reduce inflammatory signaling. Mixed / weak Most practical food/supplement adjunct, but not a strong standalone PsA joint therapy.
Curcumin / Turmeric NF-κB; JAK/STAT3; MAPK; IL-17 / IFN-γ; redox signaling Broad anti-inflammatory and signaling-modulating effects relevant to psoriatic disease biology. Very limited direct evidence Reasonable mechanistic adjunct; stronger biology than clinical PsA proof.
Boswellia / Boswellic acids 5-LOX; NF-κB; COX-2; leukotrienes Notable leukotriene / 5-LOX angle with broader anti-inflammatory effects. No strong direct PsA joint trials Plausible adjunct, especially for eicosanoid-driven inflammation.
Ginger NF-κB; COX / LOX; inflammatory pain pathways Anti-inflammatory and antioxidant actions with arthritis-relevant pathway effects. Indirect only Plausible low-to-moderate adjunct; evidence is not PsA-specific.
EGCG / Green tea catechins IL-17 / IL-23-related inflammation; oxidative stress; keratinocyte hyperproliferation Immune-regulatory and antioxidant effects; mainly supported in psoriasis/preclinical models. Mostly psoriasis / preclinical Interesting adjunct, but not proven for PsA joints.
Sulforaphane KEAP1-NRF2; oxidative stress; TH17-related inflammation; autoimmune signaling Strong redox / NRF2 rationale with anti-inflammatory effects in preclinical models. Preclinical / indirect Good mechanistic candidate for the NRF2-redox tier.
Quercetin NF-κB; PI3K/AKT/GLUT1; inflammatory cell signaling Multi-target anti-inflammatory effects with arthritis relevance. Weak direct PsA evidence Mechanistically attractive, clinically still speculative for PsA.
Resveratrol NF-κB; oxidative stress; inflammatory mediators; SIRT1/AMPK-linked effects May reduce inflammatory signaling and support metabolic/redox regulation. Very limited for PsA Interesting but not near the top for real-world PsA use.
Piperlongumine NLRP3 inflammasome; ROS-sensitive inflammatory signaling; FLS proliferation/migration; MMPs Research-stage anti-inflammatory candidate with RA/psoriasis-model relevance. Research-stage only Experimental; not a practical PsA supplement at present.
Shikonin JAK/STAT; TNF-driven synoviocyte signaling; macrophage polarization; psoriasis inflammation Biologically interesting for synovitis and immune-cell signaling. Research-stage only Experimental; mainly of mechanistic interest.


Scientific Papers found: Click to Expand⟱
1938- PL,    Piperlongumine regulates epigenetic modulation and alleviates psoriasis-like skin inflammation via inhibition of hyperproliferation and inflammation
- Study, PSA, NA - in-vivo, NA, NA
ROS↑, Apoptosis↑, MMP↓, TumCCA↑, DNAdam↑, STAT3↓, Akt↓, PCNA↓, Ki-67↓, cycD1/CCND1↓, Bcl-2↓, K17↓, HDAC↓, ROS↑, *IL1β↓, *IL6↓, *TNF-α↓, *IL17↓, *IL22↓,

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:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ki-67↓, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

K17↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

IL17↓, 1,   IL1β↓, 1,   IL22↓, 1,   IL6↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 6

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

 

Home Page